A seleção de linhagens de frangos de corte com altas taxas de crescimento e aumento de rendimento muscular vem contribuindo para o surgimento de perdas significativas na indústria avícola em decorrência de modificações anatômicas. Dentre estas alterações, destaca-se uma miopatia que se caracteriza pelo aparecimento de graus de estrias esbranquiçadas no músculo Pectoralis major, as quais seguem a direção da fibra muscular, referida como white striping. A etiologia da white striping ainda é desconhecida, mas avaliações histológicas demonstraram que esta alteração é usualmente associada à degeneração muscular e alterações miopáticas. Problemas de qualidade da carne podem ser resultantes de mudanças estruturais, morfométricas e bioquímicas do tecido muscular, com consequente alteração nas fibras musculares. Para tanto este trabalho, conduzido através de dois experimentos, teve como objetivos caracterizar histopatologicamente a miopatia white striping em diferentes graus de severidade (NORM, MOD, SEV) no músculo Pectoralis major de frangos de corte e as características morfométricas das fibras musculares, bem como avaliar a incidência desta condição em frangos de corte de linhagem Cobb abatidos aos 42 dias de idade. No primeiro experimento, a avaliação histopatológica demonstrou uma miopatia degenerativa nos graus de severidade classificados como MOD e SEV, entretanto as amostras de grau MOD apresentaram necrose ou necrose multifocal moderada, enquanto as de grau SEV apresentaram necrose difusa e acentuada, sugerindo avanço do processo degenerativo. Não foi observada proliferação de tecido conjuntivo em nenhum dos graus de white striping analisados, caracterizando este caso como de ocorrência aguda. No segundo experimento, foram verificados menor área de tecido muscular, menor diâmentro e maior densidade de fibras nos músculos Pectoralis major de frangos acometidos com white striping (MOD e SEV) quando comparado aos peitos sem esta condição (NORM). Conforme os resultados obtidos nesta pequisa, pode-se concluir que as fibras com os graus MOD e SEV de white striping demonstraram o início de um processo de regeneração muscular, de característica hiperplásica. / Genetic selection of broiler chickens for growth rate and increase of muscle yield has contributed to the appearance of significant losses in the poultry industry caused by anatomical changes. Among these alterations stands out a myophathy characterized by the occurrence of white striations on Pectoralis major muscle, seen parallel to the direction of muscle fibers, referred as white striping. The etiology of white striping is still unknown but histological changes demonstrated that this alteration is usually associated with muscle degeneration and myopatic changes. Meat quality problems may result from structural, morphological and biochemical changes of muscle tissue with consequent alterations in muscle fibers. To this study, two experiments were conducted, and aimed to histopathologically characterize the myopathy white striping at varying degrees of severity (NORM, MOD, SEV) on broilers Pectoralis major muscle and the morphometric muscle fibers characteristics as well as evaluate the incidence of this condition on Cobb 500 broiler breast fillets slaughtered at 42 days of age. The histopathological evaluation on experiment 1 showed a degenerative myopathy in both MOD and SEV degrees, however the samples classified as MOD showed microscopically necrosis or necrosis multifocal moderate, while the classified as SEV showed necrosis diffuse and strong suggesting an advancement in the degenerative process. The proliferation of connective tissue was not observed for either of the degrees of white striping investigated, characterizing this profile as an acute occurrence. In experiment 2, small area and diameter and higher densities of muscle fiber were observed in broilers Pectoralis major muscle with white striping (MOD and SEV) compared to NORM. According to the results, we can conclude that muscle fibers with white striping showed the beginning of a muscle regeneration process with hyperplasic characteristics.

Objectives: Tooth replacement therapy using endosseous implants has become an essential component of contemporary dental practice. While a plethora of factors determine clinical success, the bucco-lingual and apico-coronal dimensions of the peri-implant mucosa play an important role in both esthetics and the maintenance of peri-implant health. Studies, most of which treat mucogingival defects in the natural dentition, comparing acellular dermal matrix (ADM) and autologous subepithelial connective tissue grafts (sCTG) have shown similar clinical outcomes. The purpose of this non-inferiority trial is to determine the clinical efficacy of ADM in the augmentation of peri-implant mucosa thickness (PMT) as compared to an autologous sCTG in human adults. Methods: Twenty healthy adults treatment planned for a single tooth implant restoration in need of simultaneous peri-implant mucosa augmentation at the time of implant placement were recruited on the basis of an eligibility criteria. Patients were randomly assigned to the control group (autologous sCTG), or the experimental group (ADM allograft). Clinical measurements of mucosal thickness at the site were made with a periodontal probe and an endodontic spreader at baseline and 16 weeks post-op. These measurements were made by a masked, calibrated examiner. Gingival health, oral hygiene, wound healing and patient reported outcomes were also obtained. Mann-Whitney U tests were used to compare the mean mucosal thickness changes between the groups. Results: The mean gain in PMT was approximately 1.5mm in the control group and 0.8mm in the experimental group. When measured at 1, 3 and 5mm apical from the CEJ, only the 3mm site exhibited a difference between the groups that approached statistical significance (control: 2.08 ± 0.80mm, test: 0.83 ± 1.37mm, Mann Whitney U = 10.00, p=0.05). Changes in keratinized mucosa width, healing index and patient reported outcomes were generally similar between the two groups. Conclusions: Within the limitations of this study, both autologous sCTG and ADM appear to be adequate materials to augment PMT without sacrificing other relevant clinical parameters and/or patient related outcomes.

Abstract The increase of cardiac hemodynamic load that requires increased mechanical performance drives adaptation of the heart to maintain cardiac function. Modification of protein synthesis in cardiomyocytes allows the cells to adapt to the increased load. Cardiomyocyte hypertrophy and activation of cardiac fibroblasts over the long term is maladaptive and leads to heart failure (HF). Members of the transforming growth factor-β (TGF-β) superfamily contribute to the remodeling process. TGF-β1 acts as a paracrine messenger between cardiomyocytes and cardiac fibroblasts. Connective tissue growth factor (CTGF) modulates TGF-β signaling and plays a role in the development of fibrosis. In the current study, we aimed to investigate whether blocking the actions of CTGF could alleviate ischemic injury and reduce cardiac remodeling. We determined whether blocking the action of these ligands would modulate cardiac hypertrophy and fibrosis. In the first study, we found that antagonizing the function of CTGF protected from transverse aortic constriction (TAC) -induced left ventricular remodeling. In the second study in myocardial infarction (MI) model, blocking the function of CTGF resulted in improved post-MI survival and this prevented to the decrease in left ventricular contractile function as compared to the situation in control mice. Treatment with CTGF mAb attenuated the development of dilated cardiomyopathy and limited the increase in cardiomyocyte size and deposition of interstitial fibrosis in a remote area. In the third study, targeting the TGF-β superfamily members myostatin and activins, by administration of a soluble decoy receptor of activin receptor 2B (ACVR2B-Fc) did not affect the extent of MI injury or cardiac remodeling in MI -induced ischemic HF. Understanding the complex and converging pathways regulating cardiac remodeling is a major challenge, but it may allow for opportunities to develop new therapies, new medicines and provide new hope for people with these life-threatening diseases. / Tiivistelmä Sydämen lisääntynyt kuormitus vaatii lisääntynyttä supistusvoimaa, joka johtaa sydänlihaksen adaptaatioon pumppaustehon ylläpitämiseksi. Alkuvaiheessa sydämen liikakasvu on hyödyllistä, mutta pidempään jatkuessaan se johtaa lopulta pumppaustoiminnan heikkenemiseen ja sydämen vajaatoimintaan. Useiden signalointimekanismien on osoitettu säätelevän sydänlihaksen adaptoitumista patologisille tiloille. Transformoiva kasvutekijä –β (TGF-β) proteiiniperhe säätelee sydämen adaptoitumista sekä vasemman kammion seinämän myötäävyyttä venytykselle. TGF-β1 indusoi supistuskykyisten myofibroblastien muodostumista sekä kollageenin tuotantoa. Runsas kollageenin tuotanto vahvistaa sydämen seinämää ja on tarpeen sydäninfarktivaurion korjaamisessa, mutta pitkään jatkuessaan se heikentää sydämen toimintaa ja altistaa rytmihäiriöille, sydämen vajaatoiminnalle sekä sydänperäiselle äkkikuolemalle. Sidekudoskasvutekijä (CTGF) säätelee TGF-β1:n signalointia ja se osallistuu haavan paranemiseen sekä fibroosiin. Tutkimuksessa selvitettiin, voidaanko sidekudoskasvutekijän tai TGF-β -perheen proteiinien toimintaa estämällä lievittää sydämen vajaatoiminnan kehittymistä. Koetuloksemme osoittavat, että CTGF:n toiminnan estäminen vasta-aineen (mAb) avulla vähentää hemodynaamisen liikakuormituksen indusoimaa vasemman kammion toiminnan heikkenemistä, kammion laajenemista sekä fibroosia. CTGF mAb myös vähentää kuolleisuutta ja estää sydämen toiminnan heikkenemistä sydäninfarktin jälkeen sekä lievittää sydäninfarktin jälkeistä dilatoivan kardiomyopatian kehittymistä. Aktiviinien ja myostatiinin toiminnan esto liukoisen aktiviinireseptori 2B:n (ACVR2B-Fc) avulla sen sijaan ei vaikuta sydäninfarktivaurioon tai iskeemisen vajaatoiminnan kehittymiseen. ACVR2B-Fc kuitenkin lisää luurankolihaksen kasvua, estäen sydämen vajaatoimintaan liittyvää luurankolihaskatoa. Sydämen hypertrofian ja vajaatoiminnan syntymisen kannalta keskeisten signaalinvälitysreittien tunnistaminen ja niiden toiminnan ymmärtäminen auttaisi kehittämään tehokkaampia lääkehoitoja sydänsairauksiin.

本篇論文的主旨在研究「也」「又」「還」三個連接詞在漢語敘述文中的 篇章功能。過去對於這三個連接詞的研究，多半偏向句法和語意關係的探 討，而事實上，我們還可以從另一個角度來分析這三個連接詞，那就是探 討它們的篇章功能。研究這三個連接詞的篇章功能之前，我們首先根據 Matthiessen 和 Thompson 的模式分析了漢語句群間的凝聚關係(text relations among combined clauses)。 此一分析不僅進一步證明「也」 「又」「還」確實可以作為連接詞使用，同時更清楚地呈現出「也」「又 」「還」所連接的子句之間的關係，以及這些子句本身與其前後子句所形 成的凝聚關係。「也」「又」「還」作連接詞用時，是用來連接一組語意 相關的子句。它們都可以用來表示聯合關係；不過，「也」和「又」還可 以用來表示對照關係。表示聯合關係時，「也」連接二個或二個以上平列 的子句；「又」也是連接平列的子句，然而「又」進一步加強這些子句所 呈現的聯合關係；「還」連接帶有輕重之別的子句。至於如何知道「又」 所加強的是什麼，以及如何決定那個子句比較重，這都得依上下文而定。 表示對照關係時，「也」和「又」都是用來連接二個看似相反，而實質上 卻相輔相成的子句，差別是「又」所連接的二個子句呈現出說話者矛盾的 心理狀態。上文所提出的假設，經由我們分析書寫的語料而獲得驗證。除 此之外，我們還做了一項問卷調查，目的在測試中國人如何使用這三個連 接詞，這項問卷的結果顯示我們的假設大致正確。最後，我們依據語料的 分析及問卷結果的討論，將上文所提的假設做了小幅度的修正，使其更能 明確地說明這三個連接詞的篇章功能。

This paper describes the philosophical and functional framework of the MFA thesis exhibition Samsara Unlimited: towards an ecology of compassion. Samsara Unlimited was designed as a conceptual social artwork that would engage a network of art students and interested participants in developing a collaborative network. Using established high art aesthetics and familiar consumer based signifiers; the gallery was transformed over a week into a production, design and retail facility. In this torqued capitalist micro-system, financial profit was considered critical for the functioning of the system but secondary to the generation of a field of compassion. <p>The project sought to create a process through which the general public could become familiar with the perceptive processes engaged by artists in reconstructing everyday reality. It was posited that the ability to engage these perceptive processes would potentially lead to an ontological shift in the spectator. Participants who entered the gallery space could alter between the functional reality of a concept store and the altered reality of an art gallery. The public was encouraged to visit over the week of the installation to ask questions, get involved in art making process or simply socialize with the artists and artisans involved in the project.

This paper describes the philosophical and functional framework of the MFA thesis exhibition Samsara Unlimited: towards an ecology of compassion. Samsara Unlimited was designed as a conceptual social artwork that would engage a network of art students and interested participants in developing a collaborative network. Using established high art aesthetics and familiar consumer based signifiers; the gallery was transformed over a week into a production, design and retail facility. In this torqued capitalist micro-system, financial profit was considered critical for the functioning of the system but secondary to the generation of a field of compassion. <p>The project sought to create a process through which the general public could become familiar with the perceptive processes engaged by artists in reconstructing everyday reality. It was posited that the ability to engage these perceptive processes would potentially lead to an ontological shift in the spectator. Participants who entered the gallery space could alter between the functional reality of a concept store and the altered reality of an art gallery. The public was encouraged to visit over the week of the installation to ask questions, get involved in art making process or simply socialize with the artists and artisans involved in the project.

No description available.

Disertacijos tema: Odos kraujagyslių ir jungiamojo audinio pažeidimai sergant sistemine skleroze. Disertacijos tikslas buvo nustatyti kraujagyslių pažeidimo ir fibrozės vystymosi eiliškumą, ištiriant kraujagyslių pakitimus odoje ir jungiamajame audinyje sergantiems sistemine skleroze , su šiai patologijai būdinga kraujagyslių atrezija, bei palyginant su kitomis būklėmis, kurių metu kraujagyslių atrezijos nėra (sistemine raudonaja vilklige), bei su būklėmis, kurioms būdingas kraujagyslių funkcinis nestabilumas (Reino sindromas). Tai retrospektyvus tyrimas. Analizuota po 20 kiekvienos iš minėtų ligų sergančių ligonių ir kontrolinės grupės odos biopsijų. Be rutininių histocheminių dažymų, naudata eilė imunohistocheminių žymenų ir elektroninis mikroskopinis tyrimas. Nustatyta, kad sergantiems sistemine skleroze odoje ankščiau, negu išreikšta fibrozė pasireiškia kraujagyslių endotelio pažeidimai ir padidėjęs kraujagyslių sienelės pralaidumas. Nustatyta, kad kraujagyslių endotelio augimo veiksnio VEGF-A ir jo receptoriaus FLT-1, ir ypač HSP-47 (terminio šoko baltymo, kolagenams specifinio šaperono skatinančio fibrozę), bei eNOS (endotelio azoto sintazės) gausi ekspresija yra ankstyvos sisteminės sklerozės stadijos endotelio pakenkimo imunohistocheminiai žymenys. Taip pat nustatyta, kad ankstyvosios sisteminės sklerozės stadijos patogenezėje odoje vyrauja smulkių kraujagyslių pažeidimai. Rekomenduota naudoti odos biopsiją kaip pagalbinį diagnostinį metodą diferencijuojant tarp... [toliau žr. visą tekstą] / Dissertation topic: the damage to dermal blood vessels and connective tissue during systemic sclerosis. The aim of this dissertation was to determine the sequence in the development of vascular damage and fibrosis by studying vascular changes in the skin and connective tissue of systemic sclerosis patients with vascular atresia characteristic of this pathology and by comparing it with other conditions, where there is no vascular atresia (systemic lupus erythematosus), and with conditions, which are characterised by vascular function instability (Raynaud’s phenomenon). This was a retrospective study, which analysed 60 patients with the aforementioned diseases, 20 with each disease, and a control group of 20 skin biopsies. In addition to routine histochemical stains, a series of immunohistochemical signs and electron microscopic examination were used. It was determined that damage to the vascular endothelium and increased permeability of the vascular walls appear earlier than expressed fibrosis in the skin of systemic sclerosis patients and that the abundant expression of vascular endothelial growth factor (VEGF)-A and its receptor FLT-1 and especially HSP-47 (heat shock protein, a collagen-specific chaperone that induces fibrosis) and eNOS endothelial (nitric oxide synthase) are immunohistochemical signs of endothelial injury in the early stage of systemic sclerosis. It was determined that in the pathogenesis of the early stage of systemic sclerosis, damage to the small blood... [to full text]

Dissertation topic: the damage to dermal blood vessels and connective tissue during systemic sclerosis. The aim of this dissertation was to determine the sequence in the development of vascular damage and fibrosis by studying vascular changes in the skin and connective tissue of systemic sclerosis patients with vascular atresia characteristic of this pathology and by comparing it with other conditions, where there is no vascular atresia (systemic lupus erythematosus), and with conditions, which are characterised by vascular function instability (Raynaud’s phenomenon). This was a retrospective study, which analysed 60 patients with the aforementioned diseases, 20 with each disease, and a control group of 20 skin biopsies. In addition to routine histochemical stains, a series of immunohistochemical signs and electron microscopic examination were used. It was determined that damage to the vascular endothelium and increased permeability of the vascular walls appear earlier than expressed fibrosis in the skin of systemic sclerosis patients and that the abundant expression of vascular endothelial growth factor (VEGF)-A and its receptor FLT-1 and especially HSP-47 (heat shock protein, a collagen-specific chaperone that induces fibrosis) and eNOS endothelial nitric oxide synthase are immunohistochemical signs of endothelial injury in the early stage of systemic sclerosis. It was determined that in the pathogenesis of the early stage of systemic sclerosis, damage to the small blood... [to full text] / Disertacijos tema: Odos kraujagyslių ir jungiamojo audinio pažeidimai sergant sistemine skleroze. Disertacijos tikslas buvo nustatyti kraujagyslių pažeidimo ir fibrozės vystymosi eiliškumą, ištiriant kraujagyslių pakitimus odoje ir jungiamajame audinyje sergantiems sistemine skleroze , su šiai patologijai būdinga kraujagyslių atrezija, bei palyginant su kitomis būklėmis, kurių metu kraujagyslių atrezijos nėra (sistemine raudonaja vilklige), bei su būklėmis, kurioms būdingas kraujagyslių funkcinis nestabilumas (Reino sindromas). Tai retrospektyvus tyrimas, analizuota po 20 kiekvienos iš minėtų ligų sergančių ligonių ir kontrolinės grupės odos biopsijų. Be rutinių histocheminių dažymų naudata eilė imunohistocheminių žymenų ir elektroninės mikroskopijos tyrimas. Nustatyta, kad sergantiems sistemine skleroze odoje ankščiau, negu išreikšta fibrozė pasireiškia kraujagyslių endotelio pažeidimai ir padidėjęs kraujagyslių sienelės pralaidumas, kad kraujagyslių endotelio augimo veiksnio VEGF-A ir jo receptoriaus FLT-1, ir ypač HSP-47 (terminio šoko baltymo, kolagenams specifinio šaperono skatinančio fibrozę), bei eNOS (endotelio azoto sintazės) gausi ekspresija yra ankstyvos sisteminės sklerozės stadijos endotelio pakenkimo imunohistocheminiai žymenys. Nustatyta, kad ankstyvosios sisteminės sklerozės stadijos patogenezėje odoje vyrauja smulkių kraujagyslių pažeidimai ir į tą tikslinga atsižvelgti skiriant patogeneze pagristą sisteminės sklerozės gydymą Rekomenduota naudoti odos... [toliau žr. visą tekstą]

本研究旨在探討漢語母子對話中兒童「然後」的使用與其功能。研究語料來自於八位年齡介於兩歲七個月到五歲四個月的兒童，並分成兩組：年紀較小之兒童(平均兩歲十一個月)與年紀較大之兒童(平均四歲十個月)。本研究主要根據Su (1998)的分類，把兒童「然後」分為連接詞(connective)及言談標記(discourse marker)的使用。連接詞的使用有時間性(temporal)、遞增性(additive)、因果性(causal)及轉折性(contrast)四項功能。言談標記的使用有填補語(verbal filler)、主題接續(topic succession)及主題再開(resumptive opener)三項功能。研究結果顯示年紀較大之組的兒童使用「然後」的次數較多。隨著兒童年齡增長，言談標記使用的增加比連接詞的增加還多。「然後」當連接詞時，時間性功能使用得最多。與Yeh (2011)「然後」在敘述文中的研究比較，其顯示出「然後」在敘述文中出現得比在對話中還多。另外，時間性功能隨著年紀減少，而遞增性及因果性隨著年齡增加，可用Winskel (2003)的「概念複雜性」(conceptual complexity)來解釋。「然後」當言談標記時，兒童填補語使用得最多，其隨著年紀增加而減少使用。主題再開兩組都使用得少，而主題接續只出現在年紀較大之組別。總結，兒童在「然後」的使用上有發展上的不同。 / The study investigated Mandarin-speaking children’s different use of ranhou at different ages in mother-child conversations. Eight subjects aged from 2;7 to 5;4 were divided into two groups; a younger group (mean age: 2;11) and an older group (mean age: 4;10). In this study, the children’s use of ranhou was categorized into connective use and discourse marker use, mainly based on Su’s (1998) classification. The connective use of ranhou includes temporal, additive, causal, and contrast functions. The discourse marker use of ranhou contains verbal filler, topic succession, and resumptive opener functions. The results showed that older children used more tokens of ranhou than younger children. As children got older, the discourse marker use of ranhou increased much more than the connective use of ranhou. In the connective use of ranhou, temporal ranhou was the most frequent function. Compared with Yeh’s (2011) study of ranhou in narratives, it may be suggested that ranhou occurs more in narratives and less in conversations. Additionally, the temporal function decreased with age whereas the additive and causal functions increased with age, which could be explained by Winskel’s (2003) conceptual complexity. In the discourse marker use of ranhou, the verbal filler function was used the most and decreased with age. The tokens of the resumptive opener function were few in both groups, and the topic succession function only occurred in the older group. To conclude, the results suggest that there is a developmental difference in children’s use of ranhou.