996 resultados para Axillary web syndrome


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The study of social phenomena in the World Wide Web has been rather fragmentary, andthere is no coherent, reseach-based theory about sense of community in Web environment. Sense of community means part of one's self-concept that has to do with perceiving oneself belonging to, and feeling affinity to a certain social grouping. The present study aimed to find evidence for sense of community in Web environment, and specifically find out what the most critical psychological factors of sense of community would be. Based on known characteristics of real life communities and sense of community, and few occational studies of Web-communities, it was hypothesized that the following factors would be the most critical ones and that they could be grouped as prerequisites, facilitators and consequences of sense of community: awareness and social presence (prerequisites), criteria for membership and borders, common purpose, social interaction and reciprocity, norms and conformity, common history (facilitators), trust and accountability (consequences). In addition to critical factors, the present study aimed to find out if this kind of grouping would be valid. Furthermore, the effect of Web-community members' background variables to sense of community was of interest. In order to answer the questions, an online-questionnaire was created and tested. It included propositions that reflect factors that precede, facilitate and follow the sense of community in Web environment. A factor analysis was calculated to find out the critical factors and analyses of variance were calculated to see if the grouping to prerequisites, facilitators and consequences was right and how the background variables would affect the sense of community in Web environment. The results indicated that the psychological structure of sense of community in Web environment could not be presented with critical variables grouped as prerequisites, facilitators and consequences. Most factors did facilitate the sense of community, but based on this data it could not be argued that some of the factors chronologically precedesense of community and some follow it. Instead, the factor analysis revealed that the most critical factors in sense of community in Web environment are 1) reciprocal involvement, 2) basic trust for others, 3) similarity and common purpose of members, and 4) shared history of members. The most influencing background variables were the member's own participation activity (indicated with reading and writing messages) and the phase in membership lifecycle (from visitor to leader). The more the member participated and the further in membership life cycle he was, the more he felt sense of community. There are many descreptions of sense of community, but the present study was one of the first to actually measure the phenomenon in Web environment, and that gained well documented, valid results based on large data, proving that sense of community in Web environment is possible, and clarifying its psychological structure, thus enhancing the understanding of sense of community in Web environment. Keywords: sense of community, Web-community, psychology of the Internet

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Tutkimuksessa analysoidaan teoriatasolla web-avusteisen tiedontuottamisyhteistyön kokeilutoiminnassa esiin tulleita ongelmia ja kootaan niiden viitoittamana teoriaperustaa tulevaisuuden työskentelytavalle, tietämyksen web-avusteiselle ryhmäprosessoinnille. Keskiössä on ihminen kognitiivisena tiedonkäsittelijänä ja elinikäisenä oppijana. Organisaatiossa vallitsevat toimintastrategiat, ryhmätyöskentelyn organisointi ja ryhmässä toteutuvat käytännöt muodostavat yksilön toimintaa ohjaavan sosiaalisen toimintaympäristön, joka säätelee yhteistyöprosessin onnistumista. Yhteistyötä tarkastellaan sosiaalisen tiedonkäsittelyn ryhmäilmiönä, jossa käsite yhteistyökyky kyseenalaistuu. Tuotetussa teoriaperustassa ihminen nähdään monitasoisten oppimishaasteiden ristitulessa. Koulutuksessa vallitseva absoluuttinen tietokäsitys on pystyttävä muuttamaan konstruktivistiseksi tietokäsitykseksi: yhteistä tietämystä ryhmänä tuotettaessa yksilöiden tietämys on rakennusaineena. Koulussa saatu sosiaalisen tiedonkäsittelyn malli, itsekeskeisen tiedonkäsittelyn malli, ei sovellu tietämyksen ryhmäprosessointiin. Malliin liittyviä oppeja on poisopittava samalla kun ryhmäjäsenenä on suunniteltava ja yhdessä opeteltava ryhmäkeskeisiä ja web-avusteisia tiedonkäsittelymalleja. Näin yhteistyöprosessissa toteutuu rinnakkain asiaoppimista ja toimintaoppimista. Näitä molempia on tarpeen tukea kehitettäessä uudenlaisia web-avusteisia työskentelymenetelmiä. Osassa I esitellään tutkimuksen kokemusperäisiä virikkeitä. Suhteellisen tietokäsityksen mukaisesti tämä tutkimus on kiinteästi kytkeytynyt tutkijan elinikäiseen oppimiseen ja tutkimus kuvataan tutkijan yksilöllisen tietämyksen prosessointina. Tutkimusaiheen löytymiseen johtaneet käytännön havainnot aloittavat sen takia raportoinnin. Erityisesti koulun sosiaalisen tiedonkäsittelyn organisointi on tarkastelun kohteena. Osassa II hahmotetaan tutkimusnäkökulmaa. Tutkimuskysymykset ovat lähinnä viitoittamassa tietämyksen etsintää. Tutkimusmenetelmä, kokeilutoiminnan analysointi, on saanut vahvasti vaikutteita toimintatutkimuksesta. Tutkimusasetelman perustana on toimintaan kytkeytyvä ihmiskäsitys. Kirjallisuuden avulla etsitään mahdollisia kytkeytymiä ihmisen käyttäytymisen ja sosiaalisen toiminnan organisoinnin välillä. Osa III kuvailee tutkimusaihetta koskevan ymmärryksen prosessointia. Esiymmärrys yhteistyöstä ja yhteistyökäsitteen määrittely mahdollistavat kokeilutoimintaan ryhtymisen. Uusi viestintämahdollisuus (www) nähdään yhteisessä tiedonkäsittelyssä apuvälineenä. Käytännön kokeilujaksot tarjoavat aineksia kognitiivisen tiedonkäsittelyn syvällisten periaatteiden löytymiselle. Inhimillinen toiminta ja sosiaalinen tiedonkäsittely saavat teoriatason analysoinnissa oppimiseen perustuvia tulkintoja. Osassa IV esitellään tutkimuksen tavoitteena ollutta teoriaperustaa tietämyksen web-avusteiselle ryhmäprosessoinnille. Teoriatiivistelmässä keskiöön nousee ihmisen kognitiivinen tiedonkäsittely sekä konstruktivistisen asiaoppimisen että selviytymispainotteisen toimintaoppimisen muodossa. Sosiaalinen toimintaympäristö nähdään osallisena kognitiivisessa tiedonkäsittelyssä ja selityksenä sille, että yhteinen tiedonkäsittely ei onnistu pelkästään tietoverkkoympäristössä vaan tarvitaan myös sosiaalisia tapaamisia. Kokeilutoiminnan opetuksia tuodaan esille yhteistyöprosessin keskeisten tapahtumien tarkastelussa. Tuotettua teoriaperustaa koetellaan tieteen kentällä vertailemalla sitä muiden tutkijoiden julkaisemiin käsityksiin. Tietoverkkoteknologian suhdetta inhimilliseen tiedonkäsittelyyn verrataan muualla saatuihin ja julkaistuihin käsityksiin. Avainsanat: tietointensiivinen yhteistyö, tiedontuottamisyhteistyö, yhteistyöprosessi, yhteistyökyky, yhteistyökyvyttömyys, virtuaalinen yhteistyöorganisaatio, yksilöllinen tietämys, yhteisen ymmärryksen etsintä, yhteinen tietämys, kognitiivinen tiedonkäsittely, asiaoppiminen, toimintaoppiminen, sosiaalinen tiedonkäsittely, sosiaalinen toimintaympäristö, automatisoitunut toimintamalli, yksilökeskeinen toimintamalli, itsekeskeinen toimintamalli, ryhmäkeskeinen toimintamalli, sosiaalisen tiedonkäsittelyn toimintastrategia, työympäristössä oppiminen.

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This paper investigates the effect that text pre-processing approaches have on the estimation of the readability of web pages. Readability has been highlighted as an important aspect of web search result personalisation in previous work. The most widely used text readability measures rely on surface level characteristics of text, such as the length of words and sentences. We demonstrate that different tools for extracting text from web pages lead to very different estimations of readability. This has an important implication for search engines because search result personalisation strategies that consider users reading ability may fail if incorrect text readability estimations are computed.

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Hypertension, obesity, dyslipidemia and dysglycemia constitute metabolic syndrome, a major public health concern, which is associated with cardiovascular mortality. High dietary salt (NaCl) is the most important dietary risk factor for elevated blood pressure. The kidney has a major role in salt-sensitive hypertension and is vulnerable to harmful effects of increased blood pressure. Elevated serum urate is a common finding in these disorders. While dysregulation of urate excretion is associated with cardiovascular diseases, present studies aimed to clarify the role of xanthine oxidoreductase (XOR), i.e. xanthine dehydrogenase (XDH) and its post-translational isoform xanthine oxidase (XO), in cardiovascular diseases. XOR yields urate from hypoxanthine and xanthine. Low oxygen levels upregulate XOR in addition to other factors. In present studies higher renal XOR activity was found in hypertension-prone rats than in the controls. Furthermore, NaCl intake increased renal XOR dose-dependently. To clarify whether XOR has any causal role in hypertension, rats were kept on NaCl diets for different periods of time, with or without a XOR inhibitor, allopurinol. While allopurinol did not alleviate hypertension, it prevented left ventricular and renal hypertrophy. Nitric oxide synthases (NOS) produce nitric oxide (NO), which mediates vasodilatation. A paucity of NO, produced by NOS inhibition, aggravated hypertension and induced renal XOR, whereas NO generating drug, alleviated salt-induced hypertension without changes in renal XOR. Zucker fa/fa rat is an animal model of metabolic syndrome. These rats developed substantial obesity and modest hypertension and showed increased hepatic and renal XOR activities. XOR was modified by diet and antihypertensive treatment. Cyclosporine (CsA) is a fungal peptide and one of the first-line immunosuppressive drugs used in the management of organ transplantation. Nephrotoxicity ensue high doses resulting in hypertension and limit CsA use. CsA increased renal XO substantially in salt-sensitive rats on a high NaCl diet, indicating a possible role for this reactive oxygen species generating isoform in CsA nephrotoxicity. Renal hypoxia, common to these rodent models of hypertension and obesity, is one of the plausible XOR inducing factors. Although XOR inhibition did not prevent hypertension, present experimental data indicate that XOR plays a role in the pathology of salt-induced cardiac and renal hypertrophy.

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Gastrointestinal symptoms and impaired quality of life caused by irritable bowel syndrome (IBS) affect up to 20% of the adult population worldwide. The exact aetiology and pathophysiology of IBS are incompletely understood. Clinical studies suggest that supplementation with certain probiotics may be beneficial in IBS, but there is not enough evidence to make general recommendations. The aim of this thesis was to investigate microbiota- and mucosa-associated pathophysiological factors of IBS, and to evaluate the long-term effects of multispecies probiotic supplementation on symptoms, quality of life, intestinal microbiota and systemic inflammatory markers in IBS. The intestinal microbiota composition in IBS patients and healthy control subjects was analysed by quantitative polymerase chain reaction (qPCR). Significantly lower counts for the Clostridium coccoides and the Bifidobacterium catenulatum groups were found in IBS compared to controls. Quantitative differences also appeared in subgroup analysis based on the predominant bowel habit: diarrhoea patients harboured significantly lower numbers of Lactobacillus spp. than the constipation-predominant patients, while higher counts for Veillonella spp. were detected in constipation-predominant patients compared to healthy controls. Analysis of mucosal biopsies by a metabolomic approach revealed multiple differences between patients and controls. The most prominent finding was an upregulation of specific lipid species, principally lysophosphatidylcholines and ceramides, in IBS. The effects of multispecies probiotic supplementation with Lactobacillus rhamnosus GG, Lactobacillus rhamnosus Lc705, Propionibacterium freudenreichii subsp. shermanii JS, and Bifidobacterium breve Bb99 or Bifidobacterium animalis subsp. lactis Bb12 was evaluated in two, randomised, double-blind, placebo-controlled trials. Compared to placebo, the probiotic supplementation significantly reduced the total symptoms of IBS. No effects on bowel habit were seen. Health-related quality of life (HRQOL) is reduced in patients with IBS in comparison with the Finnish population on the whole. The probiotic supplementation improved one IBS-specific domain of quality of life (bowel symptoms), whereas no other effects on HRQOL were seen. The probiotics had no major effects on the predominant microbiota as measured by qPCR, but a microarray-based analysis suggested that the probiotic consumption stabilised the microbiota. No effects on serum sensitive-CRP or cytokines were detected. In conclusion, alterations in the microbiota composition and in the mucosal metabolite profile are potential pathophysiological factors of IBS. Multispecies probiotic supplementation alleviates the gastrointestinal symptoms of IBS, and improves the bowel symptoms domain of HRQOL. Probiotic supplementation in IBS is associated with a stabilisation of microbiota, but it does not influence systemic inflammatory markers.

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We present a novel framework and algorithms for the analysis of Web service interfaces to improve the efficiency of application integration in wide-spanning business networks. Our approach addresses the notorious issue of large and overloaded operational signatures, which are becoming increasingly prevalent on the Internet and being opened up for third-party service aggregation. Extending upon existing techniques used to refactor service interfaces based on derived artefacts of applications, namely business entities, we propose heuristics for deriving relations between business entities, and in turn, deriving permissible orders in which operations are invoked. As a result, service operations are refactored on business entity CRUD which then leads to behavioural protocols generated, thus supportive of fine-grained and flexible service discovery, composition and interaction. A prototypical implementation and analysis of web services, including those of commercial logistic systems (Fedex), are used to validate the algorithms and open up further insights into service interface synthesis.

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The growth of APIs and Web services on the Internet, especially through larger enterprise systems increasingly being leveraged for Cloud and software-as-a-service opportuni- ties, poses challenges to improving the efficiency of integration with these services. Interfaces of enterprise systems are typically larger, more complex and overloaded, with single operation having multiple data entities and parameter sets, supporting varying requests, and reflecting versioning across different system releases, compared to fine-grained operations of contemporary interfaces. We propose a technique to support the refactoring of service interfaces by deriving business entities and their relationships. In this paper, we focus on the behavioural aspects of service interfaces, aiming to discover the sequential dependencies of operations (otherwise known as protocol extraction) based on the entities and relationships derived. Specifically, we propose heuristics according to these relationships, and in turn, deriving permissible orders in which operations are invoked. As a result of this, service operations can be refactored on business entity CRUD lines, with explicit behavioural protocols as part of an interface definition. This supports flexible service discovery, composition and integration. A prototypical implementation and analysis of existing Web services, including those of commercial logistic systems (Fedex), are used to validate the algorithms proposed through the paper.

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Kasvainten, ajatellaan syntyvän yksittäisen solun perimän mutaatioista, jonka seurauksena tuon solun kasvu häiriintyy. Ruoansulatuskanavan polyyppien syntyä käytetään usein mallina siitä, miten nämä epiteelisoluun kerääntyvät mutaatiot aiheuttavat asteittain pahenevan kasvuhäiriön. Peutz–Jeghersin oireyhtymä (PJS) on perinnöllinen polypoosisyndrooma, jossa oireita aiheuttavat erityisesti maha-suolikanavan hamartomatoottiset polyypit. Noin puolella PJS potilaista havaitaan mutaatioita LKB1 kasvunrajoite geenissä. Hiirille joilta toinen Lkb1 alleeli on poistettu (Lkb1+/-) kehittyy PJS-tyypin maha-suolikanavan polyyppeja, joissa on epiteelin liikakasvun lisäksi merkittävä sileälihaskomponentti, aivan kuten PJS polyypeissa. Kuten myös muissa ruoansulatuskanavan polypooseissa, sekä PJS että hiirten polyypeissa Cyclo-oxygenaasi-2:n (COX-2) määrä on usein kohonnut. PJS-polyyppien kehittymisen molekulaarinen mekanismi on kuitenkin selvittämättä. Koska vain osa PJS potilaista kantaa LKB1 mutaatioita, mutaatiot jossakin toisessa lokuksessa saattaisivat selittää osan PJS tapauksista. Jotta PJS:n geneettinen tausta selviäisi, seulottiin kolmen LKB1:n kanssa interaktoivan proteiinin (BRG1, STRADα ja MO25α) geenit PJS potilaista joilla ei ole havaittu LKB1 mutaatioita. Yhdessäkään tutkituista geeneistä ei havaittu tautia aiheuttavia mutaatioita. Näiden kolmen geenin pois sulkeminen, ja uusien menetelmien ansiosta kasvanut havaittujen Lkb1 mutaatioden määrä viittaavat LKB1:n olevan useimpien PJS tapausten taustalla. COX-2:n estäjien käyttö on tehokkaasti vähentänyt polyyppien määrää familiaarisessa adenomatoottisessa polypoosissa. Tästä johtuen COX-2:n eston tehokkuutta tutkittiin PJS polypoosissa. PJS-tyypin polypoosin havaittin pienenevän merkittävästi Lkb1+/- hiirissä, joilta oli lisäksi poistettu toinen tai molemmat COX-2:n alleeleista. Lisäksi farmakologinen COX-2:n esto Celecoxib:lla vähensi polypoosia tehokkaasti. Näin ollen COX-2:n eston tehokkuutta tutkittiin seuraavaksi PJS potilaissa. Kuuden kuukauden Celecoxib hoidon jälkeen polypoosin havaittiin vähentyneen merkittävästi osalla potilaista (2/6). Nämä tulokset osoittavat COX-2:n roolin PJS-polyyppien kehityksessä, ja viittaavat COX-2:n eston vähentävän polypoosia. Kasvunrajoitegeenin klassisen määritelmän mukaan kasvaimen kehitys vaatii perinnöllisen mutaation lisäksi geenin toisenkin alleelin mutaation, mutta PJS-polyyppien häiriintyneestä epiteelistä ei kuitenkaan systemaattisesti löydy toista LKB1:n mutaatiota. Havainto johti tutkimukseen, jossa selvitettiin voisiko LKB1:n kasvun rajoitus välittyäkin epäsuorasti tukikudokseksi ajatelluista sileälihassoluista. Tätä tutkittiin kehittämällä poistogeeninen hiirimalli jossa Lkb1 on mutatoitunut vain sileälihassoluissa. Näille hiirille kehittyi polyyppeja, jotka ovat kaikin tavoin PJS-polyyppien kaltaisia. Lkb1:n menettäneiden solujen havaittiin tuottavan vähemmän transformoivaa kasvutekijä beetaa (TGFß), joka aiheutti solujen välisen viestinnän heikentymisen ja mahdollisesti viereisten epiteelisolujen liikakasvun. Vastaava häiriö havaittiin myös PJS-potilaiden polyypeissa, mikä viittaa siihen, että potilaillakin sileälihassolujen häiriö on polyyppien taustalla. Havainto suuntaa täten hoitokohteiden etsintää ja osoittaa että LKB1 toimii kasvunrajoittajana epätyypillisellä tavalla pitäen naapurisolujen kasvun kurissa.

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Successful identification of these factors influence upon TFS will empower stakeholders to make informed decisions as to how to best utilise the resource, boost consumer confidence thus ensuring the improved profitability of the fishery into the future.

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Most people complain about being tired and wish they could sleep in for a few more hours instead of going to work. However, 'being tired' has a whole different meaning for people living with chronic fatigue syndrome, which is also known as myalgic encephalomyelitis.

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Meckel syndrome (MKS, MIM 249000) is an autosomal recessive developmental disorder causing death in utero or shortly after birth. The hallmarks of the disease are cystic kidney dysplasia and fibrotic changes of the liver, occipital encephalocele with or without hydrocephalus and polydactyly. Other anomalies frequently seen in the patients are incomplete development of the male genitalia, club feet and cleft lip or palate. The clinical picture has been well characterized in the literature while the molecular pathology underlying the disease has remained unclear until now. In this study we identified the first MKS gene by utilizing the disease haplotypes in Finnish MKS families linked to the MKS1 locus on chromosome 17q23 (MKS1) locus. Subsequently, the genetic heterogeneity of MKS was established in the Finnish families. Mutations in at least four different genes can cause MKS. These genes have been mapped to the chromosomes 17q23 (MKS1), 11q13 (MKS2), 8q22 (MKS3) and 9q33 (MKS4). Two of these genes have been identified so far: The MKS1 gene (this work) and the MKS3 gene. The identified MKS1 gene was initially a novel human gene which is conserved among species. We found three different MKS mutations, one of them being the Finnish founder mutation. The information available from MKS1 orthologs in other species convinced us that the MKS1 gene is required for normal ciliogenesis. Defects of the cilial system in other human diseases and model organisms actually cause phenotypic features similar to those seen in MKS patients. The MKS3 (TMEM67) gene encodes a transmembrane protein and the gene maps to the syntenic Wpk locus in the rat, which is a model with polycystic kidney disease, agenesis of the corpus callosum and hydrocephalus. The available information from these two genes suggest that MKS1 would encode a structural component of the centriole required for normal ciliary functions, and MKS3 would be a transmembrane component most likely required for normal ciliary sensory signaling. The MKS4 locus was localized to chromosme 9q32-33 in this study by using an inbred Finnish family with two affected and two healthy children. This fourth locus contains TRIM32 gene, which is associated to another well characterized human ciliopathy, Bardet Biedl syndrome (BBS). Future studies should identify the MKS4 gene on chromosome 9q and confirm if there are more than two genes causing MKS Finnish families. The research on critical signaling pathways in organogenesis have shown that both Wnt and Hedgehog pathways are dependent on functional cilia. The MKS gene products will serve as excellent model molecules for more detailed studies of the functional role of cilia in organogenesis in more detail.

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Hereditary non-polyposis colorectal carcinoma (HNPCC; Lynch syndrome) is among the most common hereditary cancers in man and a model of cancers arising through deficient DNA mismatch repair (MMR). It is inherited in a dominant manner with predisposing germline mutations in the MMR genes, mainly MLH1, MSH2, MSH6 and PMS2. Both copies of the MMR gene need to be inactivated for cancer development. Since Lynch syndrome family members are born with one defective copy of one of the MMR genes in their germline, they only need to acquire a so called second hit to inactivate the MMR gene. Hence, they usually develop cancer at an early age. MMR gene inactivation leads to accumulation of mutations particularly in short repeat tracts, known as microsatellites, causing microsatellite instability (MSI). MSI is the hallmark of Lynch syndrome tumors, but is present in approximately 15% of sporadic tumors as well. There are several possible mechanisms of somatic inactivation (i.e. the second hit ) of MMR genes, for instance deletion of the wild-type copy, leading to loss of heterozygosity (LOH), methylation of promoter regions necessary for gene transcription, or mitotic recombination or gene conversion. In the Lynch syndrome tumors carrying germline mutations in the MMR gene, LOH was found to be the most frequent mechanism of somatic inactivation in the present study. We also studied MLH1/MSH2 deletion carriers and found that somatic mutations identical to the ones in the germline occurred frequently in colorectal cancers and were also present in extracolonic Lynch syndrome-associated tumors. Chromosome-specific marker analysis implied that gene conversion, rather than mitotic recombination or deletion of the respective gene locus accounted for wild-type inactivation. Lynch syndrome patients are predisposed to certain types of cancers, the most common ones being colorectal, endometrial and gastric cancer. Gastric cancer and uroepithelial tumors of bladder and ureter were observed to be true Lynch syndrome tumors with MMR deficiency as the driving force of tumorigenesis. Brain tumors and kidney carcinoma, on the other hand, were mostly MSS, implying the possibility of alternative routes of tumor development. These results present possible implications in clinical cancer surveillance. In about one-third of families suspected of Lynch syndrome, mutations in MMR genes are not found, and we therefore looked for alternative mechanisms of predisposition. According to our results, large genomic deletions, mainly in MSH2, and germline epimutations in MLH1, together explain a significant fraction of point mutation-negative families suspected of Lynch syndrome and are associated with characteristic clinical and family features. Our findings have important implications in the diagnosis and management of Lynch syndrome families.