Academic literature on the topic 'Reception capacity'

Bats are a paragon of evolutionary success. They rely on parsimonious sensory inputs provided by echolocation, yet are able to master lives in complex environments. The outer ears (pinnae) of bats are intricately shaped receiver baffles that encode sensory information through a diffraction process. In some bat species with particularly sophisticated biosonar systems, such as horseshoe bats (Rhinolophidae), the pinnae are characterized by static as well as dynamic geometrical features. Furthermore, bats from these species can deform their pinnae while the returning ultrasonic waves impinge on them. Hence, these dynamic pinna geometries could be a substrate for novel, dynamic sensory encoding paradigms. In this dissertation, two aspects of this dynamic sensing process were investigated: (i) Do local shape features impact the acoustic effects during dynamic deformation of the bat pinna? and (ii) do these shape deformations provide a substrate for the dynamic encoding of sensory information? For this, a family of simplified biomimetic prototypes has been designed based on obliquely truncated cones manufactured from sheets of isobutyl rubber. These prototypes were augmented with biomimetic local shape features as well as with a parsimonious deformation mechanism based on a single linear actuator. An automated setup for the acoustic characterization of the time-variant prototype shapes has been devised and used to characterize the acoustic responses of the prototypes as a function of direction. It was found that the effects of local shape features did interact with each other and with the deformation of the overall shape. The impact of the local features was larger for bent than for upright shape configurations. Although the tested devices were much simpler than actual bat pinnae, they were able to reproduce numerical beampattern predictions that have been obtained for deforming horseshoe bat pinnae in a qualitative fashion. The dynamically deformable biomimetic pinna shapes were estimated to increase the sensory encoding capacity of the device by unit[80]{%} information when compared to static baffles. To arrive at this estimate, spectral clustering was used to break up the direction- and deformation-depended device transfer function into a discrete signal alphabet. For this alphabet, we could estimate the joint signal entropy across a bending cycle as a measure for sensory coding capacity. The results presented in this thesis suggest that bat biosonar posses unique dynamic sensing abilities which have no equivalent in man-made technologies. Sensing paradigms derived from bat biosonar could hence inspire new deformable wave-diffracting structures for the advancement in sensor technology.<br>Ph. D.

Cognitive radios have been proposed as a new technology to counteract the spectrum scarcity issue and increase the spectral efficiency. In cognitive radios, the sparse assigned frequency bands are opened to secondary users, provided that interference induced on the primary licensees is negligible. Cognitive radios are established in two steps: the radios firstly sense the available frequency bands by detecting the presence of primary users and secondly communicate using the bands that have been identified as not in use by the primary users.<p><p>In this thesis we investigate how to improve the efficiency of cognitive radio networks when multiple cognitive radios cooperate to sense the spectrum or control their interferences. A major challenge in the design of cooperating devices lays in the need for exchange of information between these devices. Therefore, in this thesis we identify three specific types of control information exchange whose efficiency can be improved. Specifically, we first study how cognitive radios can efficiently exchange sensing information with a coordinator node when the reporting channels are noisy. Then, we propose distributed learning algorithms allowing to allocate the primary network sensing times and the secondary transmission powers within the secondary network. Both distributed allocation algorithms minimize the need for information exchange compared to centralized allocation algorithms.<br>Doctorat en Sciences de l'ingénieur<br>info:eu-repo/semantics/nonPublished

This study aims to investigate challenges within the provision of integration support to quota refugees and municipal integration staffs understanding of these challenges in Skåne. It was conducted through questionnaires and semi-structured interviews with municipal integration staffs in Skåne. The research findings indicate three key challenges in the reception of quota refugees namely lack adequate housing, lack of financial resources from the region and government, and lack of provision of psychosocial support. Further challenges are connected to the lack of translators available to municipalities in the quota refugees’ mother tongue, the lack of English or major refugee languages among quota refugees, and often poor mental health which slow down Swedish language learning process and affect integration negatively. As its contribution, this study provides a broader view on challenges with the provision of integration support by municipalities regarding reception capacity, housing, and integration programs to quota refugees simultaneously. Thereby, it points out the differences among municipalities in terms of resource allocation for integration, as well as the political will to integrate quota refugees which create unequal chances for integration.

The University of Manchester, PhD by Published Work, 2018 For several reasons, small and medium enterprises (SMEs) are an important group of firms. In most market economies SMEs contribute significantly to wealth and job creation, economic growth, and product and service innovation. At the same time, SMEs are said to produce environmental impacts that are significant and that need managing and regulating. Their importance, from an economic and environmental perspective, is reflected in the fact that SMEs have become an established subject for research, with a distinct area of analysis focusing on how they manage their environmental impacts. Despite considerable interest in this area, aspects of their behaviour are in need of further examination, for there are still misunderstandings and gaps in knowledge. An area where gaps exist is how SMEs respond to different forms of environmental regulation (e.g., command-based or market-based approaches) and different forms of regulatory pressure (e.g., such as those pressures from civil society that might induce compliance-related activities or market forces that might flow through, and affect, the value chain). Why the gaps? On the one hand, and generally speaking, a common claim among those who have considered issues affecting smaller firms is that regulation is an important driver of environmental behaviour. There is a well-documented set of linked claims and empirical findings that smaller firms tend to be motivated by compliance with regulatory standards, yet owing to their scarce resources can find themselves hovering on the edge of compliance. Typically, SMEs will attempt to do no more than the law requires of them. They tend not, as it were, to go beyond compliance. Of course, this is an important observation - one that might say much, even if indirectly, about the motivations and intentions of smaller firms. It might indicate that SMEs, rather than addressing environmental issues, are more concerned with making cost savings and efficiency gains, or with satisfying the requirements of customers over such matters as product or service quality and delivery. While significant, there are at least three reasons why this view remains incomplete as an explanation for the interaction between SMEs, regulation and the environment. Firstly, this view tends to over-homogenise smaller firms. By treating them as a standardized group, the inference is that SMEs view and respond to regulation - i.e., they are all driven by regulation - in a broadly similar way. Secondly, it says little about how and why regulation drives behaviour. Claiming that regulation drives behaviour is helpful, but the claim is unduly narrow and leaves several important questions. In what ways does regulation drive behaviour? Does regulation drive all smaller firms in the same way? Thirdly, and finally, it suggests that different forms of regulation drive SME behaviour and that different forms of regulation drive this behaviour in broadly similar ways. That is, it is incomplete as it lacks appreciation of the widening scope of regulation and governance, and the nature of smart mixes of regulation. It fails to properly consider whether and how SMEs might respond differently to command-based regulation, market- or information-based measures, or self- or so-called civil regulatory pressures. On the other hand, and again in general terms, while those who have examined regulation have looked at how it can influence firms, they have tended to pay too little regard to how firms of different size may respond to different approaches or to how the factors and characteristics relating to size may shape the effectiveness of regulation. SMEs particularly are often discussed as an unusual sideshow that might raise different issues in relation, say, to the impacts of regulation on performance or innovation. That we often pay too little regard to how firms of different size may respond raises difficulties, particularly given our increasing understanding that there is no guarantee that a particular instrument will work in all situations. In other words, we are becoming more aware of the fact that the effectiveness or ineffectiveness of regulation is likely to be context-sensitive, and that the size of the enterprise is likely to be an important determinant of context. This thesis does take, and provides evidence for, the view that the organisational context is crucial to understanding how regulation functions. The thesis does not claim to provide all answers, but it does adopt the position that, in aggregate terms, a firm's size, or the factors that can be associated with size (e.g., resources, skills, knowledge, visibility, profile, stakeholder relations), and related factors concerning a firm's mind-set, can affect two things; first, the types of regulatory influences that may affect organizational behaviour and, second, how firms will respond to those influences. By focusing on SMEs, the thesis in some ways reinforces the dominant view that regulation is a driver of behaviour. Nevertheless, it goes much farther than this by showing, both theoretically and empirically, that there are important differences across SMEs and that these differences determine how and why they respond to regulation. It extends the common view by showing how SMEs differ not only in terms of the types of regulatory influences that shape their behaviour, but also in terms of how they react to these different influences. The emerging picture thus shows that the responses of firms are determined by their particular characteristics. The term used in this thesis is 'receptive capacity', which is shown to be a composite measure that includes the capabilities (e.g., resources, skills, knowledge) and orientations (e.g., views) of firms. It is suggested here that the range of receptive capacities across firms is enormous, since no two firms will be identical. Yet, it is argued - and demonstrated - that firms can be grouped according to certain identifiable characteristics, and that these groups of firms will respond to regulatory pressures in broadly similar ways; that is, there are groups of firms that have broadly similar resources and broadly similar worldviews. Thus, as well as suggesting that differences can be found at the micro level, it is demonstrated that there are sufficient commonalities across some firms that we can understand them as groups - groups of individual firms with some common characteristics. In conclusion, it is the differences across firms that provide us with a more sophisticated view of how SMEs are influenced by, and respond to, regulation. It is the nature of differences that is the main contribution of this research to both the fields of regulation and organisational and management studies. It is suggested finally that these differences have implications for how we design regulation, for how we may expect regulation to work or indeed not work, and for issues such as regulatory complexity and smart mixes.

ERRα est un récepteur nucléaire dont l’activité est controlée par des co-régulateurs transcriptionnels. La forte expression de ERRα dans les cancers est corrélée à un mauvais pronostic. Les mécanismes par lesquels ERRα régule la migration des cellules cancéreuses sont mal compris, tout comme les co-régulateurs impliqués. Nous avons identifié deux enzymes modificatrices d’histone, LSD1 et SET7, agissant comme régulateurs positifs de ERRα.I. ERRα modifie les activités biochimiques de la déméthylase LSD1 vers la déméthylation (activatrice) de H3K9me2. L’activation des cibles de ERRa-LSD1 (identifiées par RNA-Seq) requiert le recrutement de ce complexe aux sites d’initiation de la transcription (TSSs), réalisé par le facteur de transcription NRF1 qui, lui, ne régule pas l’activité enzymatique de LSD1.II. Un autre groupe de cibles de ERRα (identifié par RNA-Seq) est sous le contrôle de l’histone méthyltransférase SET7 qui mono-méthyle H3K4. Le recrutement de SET7 aux TSSs est contrôlé par le facteur de transcription ETS1, qui promeut les interactions entre SET7 et ERRα, conduisant à l’activation de l’expression des gènes en aval.Des analyses par Gene Ontology ont montré que les cibles communes de ERRα/LSD1 et de ERRα/SET7 sont fortement enrichies en termes d’invasion cellulaire. De manière cohérente, la déplétion individuelle de chacun de ces facteurs (et également celle de NRF1 ou ETS1) réduit les capacités d’invasion, observée en tests in vitro (transwell) ou in vivo par xénogreffe sur embryons de poisson-zèbre.En résumé, nos résultats montrent deux réseaux de régulation impliquant des modifications d’histone induites par ERRα, conduisant à l’invasion cellulaire<br>ERRα is a nuclear receptor whose activity mainly depends on its interaction with transcription co-regulators. High levels of ERRα are found in various cancer types and correlate with poor prognosis. However, the mechanisms linking ERRα to cancer cell migration as well as the coregulators involved are unclear. In our study, we found two histone-modifying enzymes, LSD1 and SET7, acting as positive regulators of ERRα.I. ERRα impacts the biochemical activities of the LSD1 demethylase. Activation of ERRα -LSD1 targets (identified by RNA-Seq) requires the recruitment of this complex at Transcriptional Start Sites (TSSs), which is achieved by the NRF1 transcription factor. In our study, we have shown several points: NRF1, but not ERRα , is involved in positioning LSD1 to TSS, whereas ERRα , but not NRF1, regulates LSD1 enzymatic activities towards demethylating H3K9me2.II. A distinct group of ERRa target genes (identified by RNA-Seq) is under the control of the histone methyltransferase SET7 which mono-methylates H3K4. Appropriate recruitment of SET7 at TSSs is controlled by the ETS1 transcription factor, promoting the interaction between SET7-ERRa, leading to target gene expression.Gene Ontology analysis revealed that ERRa-LSD1 co-targets, as well as ERRa-SET7 co-targets, are enriched in terms of cell invasion. Consistently, depletion of each of these factors, as well as depletion of NRF1 or ETS1, leads to reduced cell invasion capacities as observed in transwell assays or in vivo, using xenotransplantation in the zebrafish embryo.Altogether, our results show two regulatory networks involving histone modifications induced by nuclear receptors, leading to increased cell invasion

The main expansion of the discovery of genetic variants associated with complex diseases has occurred during the last decade. This expansion has been accompanied, and in some sense motivated, by the desire to use this information to improve the predictive capacity of many diseases with an unidentified familial component, including coronary heart disease (CHD), with the aim of translating this genetic knowledge into clinical practice. This doctoral thesis is structured in two lines of investigation that address distinct aspects of this issue, first to evaluate the possible role of genetic variation in a candidate gene in modulating CHD risk, and second to evaluate whether genetic information can be used to improve risk assessment tools used in clinical practice. In the first research line (described in Part I), we investigate the contribution of genetic variation in one of the most widely-studied genes in cardiovascular genetics, ESR1, which encodes the Oestrogen receptor α protein. We provide a solid meta-analysis of evidence regarding the most widely-studied variant in this gene and we further explore the role of a broad range of common and uncommon variants in this gene in CHD risk. Using these approaches, we find no evidence of association between the genetic variants studied and CHD risk. However, although we can confidently accept that common genetic polymorphisms are not associated with cardiovascular disease, we cannot discard the possibility that other types of variation in this gene (for instance epigenetic variation) could modify susceptibility to cardiovascular disease, or that other elements of this pathway are associated with an increased risk of CHD. In this research I have provided a reliable answer to this long running unanswered question in cardiovascular genetics, allowing research to re-focus on other elements of this system or other pathways. In the second line, we explored the possible utility of genetic information obtained from genome-wide association studies (GWAS) in prediction of 10-year risk of CHD events by adding this information to cardiovascular risk functions. We have followed the recommendations proposed by the American Heart Association for evaluating the utility of novel biomarkers in clinical practice, and have demonstrated that although the magnitudes of the effects of these genetic variants on CHD risk are modest, there is a tendency towards improvement in the capacity of the risk functions to predict future CHD events. The translation of genetic information into clinical practice was one of the main motivations for the investment in genome-wide association studies, and my research represents one of the first efforts to explore this possibility.<br>L’expansió principal pel que fa al descobriment de variants genètiques associades amb malalties complexes s’ha dut a terme durant la última dècada. Aquesta expansió ha estat acompanyada, i d’alguna forma motivada, pel desig d’usar aquesta informació per millorar la capacitat de predicció d’aquelles malalties on hi és present un cert component familiar però en les que no es coneixien les variants que conferien un major risc de patir la malaltia, entre elles la cardiopatia isquèmica (CI). La present tesis doctoral està estructurada en dues línies d’investigació que avaluen el possible rol d’un gen candidat en la susceptibilitat de la CI i també avalua la millora en la capacitat de predicció d’un esdeveniment coronari de les eines usades habitualment en la pràctica clínica mitjançant la inclusió d’informació genètica. Més concretament, la primera línea d’investigació es centra en la contribució de la variació genètica en un dels gens més estudiats en relació amb CI: el gen que codifica pel receptor d’estrogens alfa (ESR1). En aquesta línea hem proveït un sòlid meta-anàlisis entre la variant més àmpliament estudiada d’aquest gen i risc coronari i també hem explorat el paper de la majoria de les variants comunes descrites en aquest gen i risc de CI. Mitjançant cap dels anàlisis hem trobat evidència d’associació entre les variants genètiques en aquest gen i el risc de CI. No obstant això, i encara que podem acceptar que les variants genètiques comunes d’aquest gen no estan associades amb esdeveniments coronaris, no podem descartar que altres tipus de variació en aquest gen (com per exemple variació epigenètica) pugui estar modificant la susceptibilitat a patir un esdeveniment coronari, ni tampoc que altres elements de la mateixa cadena de senyalització estiguin associats amb la malaltia. En la segona línea d’investigació, hem explorat el possible paper de les variants genètiques, obtingudes mitjançant estudis d’associació global del genoma (GWAS), en la millora de la capacitat de predicció a 10 anys dels esdeveniments coronaris, mitjançant la seva addició en les funcions de risc cardiovascular clàssiques. Hem seguit les recomanacions proposades per la American Heart Association per l’avaluació en la pràctica clínica de nous biomarcadors, i hem demostrat que, tot i que la magnitud de l’associació d’aquestes variants és modesta, hi ha una tendència cap a la millora de la capacitat de predicció de les funcions de risc.

An important obstacle to a functional cure for HIV/AIDS is the persistence of viral reservoirs found throughout the body in various cells and tissues. Reservoirs can be latently infected cells, or in the case of follicular dendritic cells (FDC), non-infected cells that trap infectious virus on their surface through immune complexes (HIV-IC). Although several strategies have been employed to target and eliminate viral reservoirs, they are short-lived and ineffective. In an attempt to provide a long-term approach, chimeric antigen receptor T (CAR-T) cells were designed to eliminate native HIV on FDCs. Although effective at eliminating HIV-infected cells, and halting spreading infection, their ability to eliminate the viral reservoir found on (FDCs) remains unclear. We used a novel second-generation CAR-T cell expressing domains 1 and 2 of CD4 followed by the mannose binding lectin (MBL) to allow recognition of native HIV envelope (Env) to determine the capacity to respond to the viral reservoir found on FDCs. We employed a novel fluorescent lysis assay, the Carboxyfluorescein succinimidyl ester (CFSE) release assay, as well as flow cytometric based assays to detect functional CAR-T activation through IFN-γ production and CD107a (i.e., LAMP1) membrane accumulation to test cytolytic capacity and functional activation of CD4-MBL CAR-T cells, respectively. We demonstrated their efficacy at eliminating HIV-infected cells or cells expressing gp160. However, these CAR-T cells were unable to lyse cells bearing surface bound HIV-IC. We found that failed lysis was not a unique feature of a resistant target, but a limitation in the CAR-T recognition elements. CAR-T cells were inactive in the presence of free HIV or in the presence of concentrated, immobilized virus. Further experiments determined that in addition to gp120 recognition by the CAR-T, the adhesion molecule ICAM-1 was necessary for efficient CAR-T cell killing of HIV-infected cells. CAR-T cell activity and killing were inhibited in the presence of ICAM-1 blocking antibody. These results suggest that other factors, such as adhesion molecules, play a vital role in CAR-T responses to HIV-infected cells. In addition, our findings highlighted the necessity to consider all models of HIV reservoirs, including FDCs, when evaluating therapeutic efficacy.

The Toll-like receptor (TLR) family plays a crucial role in innate immunity by mediating the recognition of, and response to a variety of microorganisms. Dysregulation of TLR-mediated inflammatory responses may, however, lead to a variety of acute and chronic inflammatory conditions. The description of a naturally occurring soluble form of TLR2 (sTLR2), and the observation that sTLR2-depleted serum renders leukocytes hypersensitive to TLR2-mediated stimulation, demanded a full assessment of sTLR2's regulatory capacity and an investigation of the underlying mechanism and therapeutic potential. The present study addressed these issues, and reports that cells overexpressing sTLR2, or stimulated in the presence of the sTLR2 protein, are TLR2 hyposensitive. Regulation was TLR2-specific, affected NF-kB activation, phagocytosis and superoxide production. Mice administered sTLR2 with Gram-positive bacteria-derived components showed lower levels of the neutrophil (PMN) chemoattractant, keratinocyte-derived chemokine lower PMN numbers and late apoptotic PMN. Mononuclear cell recruitment was not affected, and endogenous peritoneal sTLR2 levels increased. Notably, the anti-inflammatory effect of sTLR2 did not compromise the capacity of mice to clear a live infection. sTLR2 interfered with the mobilisation of TLR2 to lipid rafts, acted as a decoy receptor, and disrupted the receptor (TLR2)-co-receptor (CD 14) interaction by associating with CD 14. In order to identify the region(s) of sTLR2 involved in the interaction with CD 14, the leucine-rich repeats (LRRs) of TLR2 were mutated, and the ability of these mutants to affect CD 14- dependent signalling was evaluated. Peptides representing the LRR6 and LRR20 were found to specifically inhibit CD14-dependent TLR2 triggering, indicating that these LRRs are directly involved in the TLR2-CD14 interaction. This study defines sTLR2 as an efficient regulator of TLR2-mediated inflammatory responses. The capacity of sTLR2 and TLR2-derived peptides to exert regulatory effects by targeting CD 14 may inform the design of therapeutics against inflammatory conditions that will aim at disrupting the co-receptor's activity, thus blunting, but not abrogating, microbial recognition and host responses.

Abstract Billions of reared fish are released to the wild to compensate e.g. for the loss of natural populations. However, the efficiency of the releases is low. It has been proposed that one of the factors affecting the low survival rate of reared fish is their low swimming capacity. The molecular, metabolic and structural characters of muscle fiber define the swimming capacity of fish. Swimming capacity is related to the ecological competence of the fish, including the ability to complete long migrations and catch pray. One of the aims of the current study is to compare the properties of muscles of reared and wild salmon. The second aim of the study is to alter the muscular parameters of reared fish closer to those of wild fish by means of training. The muscular differences between wild, reared and trained fish are analyzed with immunological, histochemical and electron microscopic methods. The main focus is on the dihydropyridine and ryanodine receptors. These receptors are involved for example in the initiation, force and velocity of muscle contraction. According to the results, the level of receptors is higher in the muscles of wild as compared to reared fish. The aerobic ATP production capacity is also higher in the wild fish. However, with training both the level of receptors and oxidative capacity of reared fish increase. Moreover, the swimming capacity is enhanced in trained fish, and there is a connection between the level of receptors and swimming capacity of fish. Training also affects the migration pattern of fish which starts to resemble more that of wild fish. In conclusion, the results of the current study show that the performance of fish as a whole depends on functional parameters at cellular level. For the first time, it is shown that the level of receptors involved in muscular contraction is low in muscles of reared fish. However, the muscular properties are not definite. It is now shown that with training, both the muscular and migration parameters of reared fish approach those of wild fish. This will most probably increase the survival probability of trained, reared fish in the future<br>Tiivistelmä Kalojen kasvatus ja istutus takaisin luontoon on yksi tärkeimmistä keinoista säädellä ja palauttaa kalakantoja vesistöihin. Maailmanlaajuisesti puhutaan miljardien kalojen istutusmääristä vuosittain. On kuitenkin hyvin tunnettu tosiasia, että kasvatetut kalat eivät selviä luonnossa yhtä hyvin kuin villit lajikumppaninsa. On arvioitu, että vain alle 5 % istutetuista kaloista selviää lisääntymisikään asti hengissä. Eräs tekijä, joka voi vaikuttaa kalojen selviytymiseen, on kalojen lihaskunto. Kasvatettujen kalojen uintikyvyn on todettu olevan heikko villeihin lajikumppaneihin verrattuna. Luonnossa kaloilta kuitenkin vaaditaan suurta uintikykyä esim. saalistukseen, pedoilta pakenemiseen ja vaellukseen. Eräs tämän työn päätavoitteista on määrittää, miten kasvatettujen ja villien kalojen lihasten molekulaariset, aineenvaihdunnalliset ja rakenteelliset ominaisuudet poikkeavat toisistaan, jotta voidaan arvioida mitkä solutason tekijät vaikuttavat kalojen uintikykyyn ja sitä kautta selviytymiseen. Toisaalta kasvatettujen kalojen lihasten toiminnallisten tekijöiden tasoja pyritään nostamaan harjoittelun avulla lähemmäksi villien vastaavaa ja täten vaikuttamaan kasvatettujen kalojen uintikykyyn ja sitä kautta lopulta selviytymiseen. Työssä lihasten ominaisuuksia analysoidaan immunologisin, histokemiallisin ja elektronimikroskooppisin menetelmin. Tutkimuksissa keskitytään erityisesti dihydropyridiini- ja ryanodiinireseptorien suhteellisiin määriin. Nämä reseptorit osallistuvat lihasten supistumisen aikaansaatiin ja niiden määrä korreloi positiivisesti lihasten voiman ja supistumisnopeuden kanssa. Tulosten mukaan villien kalojen lihaksissa on huomattavasti enemmän reseptoreita verrattuna kasvatettujen kalojen lihaksiin. Myös aerobinen ATP:n tuottokapasiteetti on villeillä kaloilla huomattavasti tehokkaampaa. Harjoittelun jälkeen kasvatettujen kalojen lihasten reseptorimäärät ja aerobinen kapasiteetti kuitenkin kasvavat lähemmäksi villien vastaavaa. Lisäksi lihasten reseptorimäärä ja uintikapasiteetti näyttävät korreloivan keskenään. Harjoittelun seurauksena kasvatettujen kalojen vaellusnopeus, eräs kalojen selviytymiseen vaikuttavista tekijöistä, muistuttaa myös enemmän villien vastaavaa. Yhteenvetona voidaan sanoa, että kalojen koko suorituskyky riippuu lihasten solutason mekanismien tehokkuudesta. Tässä työssä todettiin ensimmäistä kertaa, että kasvatettujen kalojen lihaksissa niiden reseptoreiden määrät, jotka liittyvät itse lihassupistuksen tehokkuuteen, ovat huomattavasti alemmat kuin villeillä. Lihasten toiminnalliset ominaisuudet eivät kuitenkaan ole muuttumattomia vakioita. Tulosten perusteella harjoitettujen kalojen sekä lihas- että vaellusominaisuudet lähestyvät villien vastaavaa. Tämä harjoittelun jälkeinen muutos lisää todennäköisesti kasvatettujen kalojen selviytymismahdollisuuksia