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Sağlık iletişimi etki ve kapsamı anlaşıldığından beri çok önemli bir alan olarak algılanmaktadır. Sağlık personeli ve hastalar arasında yaşanan iletişim problemlerinin çözümü ya da başarılı bir kişilerarası iletişim sürecinin devamı gibi konuların yanı sıra, sağlık alanında kamuoyunu doğru bilgilendirmek de bu alanda araştırılan konular arasına girmektedir. Bu çalışmanın temel amacı da popüler kültür metinleri olarak ifade edilen capslerde mizah yoluyla sağlık konulu mesajların yayılımını incelemektir. Hareketli görseller ya da sadece imaj üzerine yazılı metin olarak ortaya çıkan capslerin yaratıcılarının temel amacı gündemde yer eden konuya ilişkin kanısını paylaşıma açmak, yayılımını sağlamak ve etkileşim oluşturmaktır. Ancak capslerin söylemsel düzeyde incelendiğinde gülmenin yanı sıra düşündüren imgeler taşıdığı ifade edilebilir. Bu anlamda çalışmada sağlık alanında marka olma özelliği taşıyan ve sürekli söylemleri ile medyada yer eden Kalp ve İç Hastalıkları Profesörü Canan Karatay'ın internet ortamında yayılan capsleri incelenerek söylemlerin arasına gizlenen anlamlar ortaya çıkarılmaktadır. Çalışmada temelde bireyleri ikna etme sürecini en iyi açıklayan modellerden biri olarak kabul edilen Ayrıntılandırma Olasılığı Modelinde (ELM) çevresel yol ipuçları taşıyan mizahın görsel/söylemsel düzeyde kullanımı incelenmiştir. Çalışma bu anlamda hedef kitlenin dikkatini çekme, hedef kitleyi etkileme aracı olarak mizahın da kullanılabileceğini ortaya koymak açısından önemlidir., Healthcare field communication has been considered as an important field since its effect and content was understood. Apart from issues like the solution of the communication problems between healthcare personnel and patients or maintaining a successful inter personal communication; informing the public regarding healthcare field are among discussed topics. The main aim of this study is to examine the propagation of health related messages sent via captions which are mentioned as popular culture texts. The basic purpose of the creators of these captions which emerge as written texts on moving visuals or only on images is to share their views on a current topic, spread the topic and create an interaction. However, when these captions are examined in discursive level it can be stated that they make people think as well as laugh. In this regard, this study aims to analyze Cardiac and Internal Diseases Professor Canan Karatay's internet captions, who is a brand in her own field and who is popular with theme dia with her speeches, and to reveal the means hidden in these speeches. In this study, essentially Elaboration Likelihood Model (ELM) is considered as one of the models that explains the process of convincing individuals and with ELM it is researched the humour is used in visual/discursive level as a peripheral way. This study is important in terms of revealing that humour can be used to gain attention of and affect the target population.

Sosyal medyanın erişim ve etkileşimdüzeyi reklam ve pazarlamacılar için bu mecrayı cazip hale getirmektedir.Özellikle reklamcılar için sosyal platformların hukuki yapısının henüzoluşturulmamış olması ve yaratıcılıkta diğer mecraların geride bırakan uygulamalarınyer alması sosyal medyayı daha tercih edilir kılmaktadır. Erişim kolaylığınedeniyle hızla toplumsal hayatımızda yer alan sosyal ortamlar zamanla birtakım etik sorunları da beraberinde getirmektedir. Kullanıcılara ait verileringüvenliğinin sağlanamamasından, bireylerin istem dışı reklamlara maruzkalmasına kadar birçok etik problem üzerinde tartışılmaktadır. Çevrimdışıreklam anlayışından farklı olarak reklam olduğu açıkça belirtilmeyen,içeriklerin içine gömülen reklam uygulamaları gizli reklam olarak ifadeedilmektedir.Araştırmada hala hukuksal yapısıoluşturulmamış sosyal medyada reklam etiği ihlallerinden gizli reklamkullanımını örneklem üzerinden ortaya koymak amaçlanmaktadır. Teknik kadro yönetiminde kurgusal olarak tasarlanangündemden haberlerin, kültürel ve eğlenceli içeriklerin yer aldığı Stolk veVibio isimli YouTtube kanallarının videoları incelenmiş içerik yöntemi ilevideolarda yer alan gizli reklamlar analiz edilmiştir. Video akışı içindereklamların ve reklamda yer alan markanın/ürünün reklam olduğu anlaşılmayacakşekilde veriliş şekli ortaya konmuştur. Çalışma sosyal medyada reklam etiğiproblemleri üzerinde çalışan diğer araştırmacılara ve kontrol mekanizmasınıngerekli olduğunu savunan karar mekanizmalarına yön vermede önemtaşımaktadır., Social media’s level of access and interaction makesthis channel attractive for advertisers and marketers. The fact that the legal structure ofsocial platforms has not yet been established and its incorporatingapplications that are ahead of other channels in terms of creativity makessocial media more preferable, especially for advertisers. Social environmentsthat quickly take place in our lives thanks to their accessibility also bring anumber of ethical problems along with them. Many ethical issues from notensuring the security of user data to individuals’ being exposed to unwantedadvertisements are being discussed. Unlike traditional advertising,advertisements which are not explicitly addressed and embedded within contentsare referred as hidden advertisements. In this study, it is aimed to reveal the case study ofhidden advertising the violations of advertising ethics in the social media,which are not still legalized, through the sample. Videos from YouTubechannels, Stolk and Vibio, where news from the agenda, cultural andentertaining contents are fictionally designed by a technical staff managementare examined and the hidden advertisements in the videos are analyzed throughcontent analysis. The way in which the advertisements and the brand / productincluded in the advertisement within the video stream are presented. The studyis important in terms of guiding other researchers working on ethical issues inthe social media advertising and the control mechanisms that advocate the need for adecision-making mechanism.

Graphical abstract, Background & Aims Intrahepatic granuloma formation and fibrosis characterize the pathological features of Schistosoma mansoni infection. Based on previously observed substantial anti-fibrotic effects of 24-nor-ursodeoxycholic acid (norUDCA) in Abcb4/Mdr2−/− mice with cholestatic liver injury and biliary fibrosis, we hypothesized that norUDCA improves inflammation-driven liver fibrosis in S. mansoni infection. Methods Adult NMRI mice were infected with 50 S. mansoni cercariae and after 12 weeks received either norUDCA- or ursodeoxycholic acid (UDCA)-enriched diet (0.5% wt/wt) for 4 weeks. Bile acid effects on liver histology, serum biochemistry, key regulatory cytokines, hepatic hydroxyproline content as well as granuloma formation were compared to naive mice and infected controls. In addition, effects of norUDCA on primary T-cell activation/proliferation and maturation of the antigen-presenting-cells (dendritic cells, macrophages) were determined in vitro. Results UDCA as well as norUDCA attenuated the inflammatory response in livers of S. mansoni infected mice, but exclusively norUDCA changed cellular composition and reduced size of hepatic granulomas as well as TH2-mediated hepatic fibrosis in vivo. Moreover, norUDCA affected surface expression level of major histocompatibility complex (MHC) class II of macrophages and dendritic cells as well as activation/proliferation of T-lymphocytes in vitro, whereas UDCA had no effect. Conclusions This study demonstrates pronounced anti-inflammatory and anti-fibrotic effects of norUDCA compared to UDCA in S. mansoni induced liver injury, and indicates that norUDCA directly represses antigen presentation of antigen presenting cells and subsequent T-cell activation in vitro. Therefore, norUDCA represents a promising drug for the treatment of this important cause of liver fibrosis.

WOS: 000346144500010, In this study, calpastatin (CAST) gene polimorphism was investigated in 7 native sheep breeds reared in Turkey by using PCR-RFLP method. The frequencies of M and N alleles of CAST gene in Kangal (n= 31), Awassi (n= 26), Guney Karaman (n= 23), Akkaraman (n= 21), Morkaraman (n= 34), Karayaka (n= 33), and Karakas (n= 22) sheep breeds were determined as 0.92-0.08, 0.59-0.41, 0.67-0.33, 0.69-0.31, 0.87-0.13, 0.86-0.14, 0.89-0.11 respectively. According to chi-square test, all the other populations were consistent with Hardy-Weinberg equilibrium, whereas Morkaraman, Ivesi and Karayaka populations showed significant (P

Multiple sclerosis (MS) is the most common autoimmune disease affecting the central nervous system. It is characterized by auto-reactive T cells that induce demyelination and neuronal degradation. Treatment options are still limited and several MS medications need to be administered by parenteral application but are modestly effective. Oral active drugs such as fingolimod have been weighed down by safety concerns. Consequently, there is a demand for novel, especially orally active therapeutics. Nature offers an abundance of compounds for drug discovery. Recently, the circular plant peptide kalata B1 was shown to silence T-cell proliferation in vitro in an IL-2-dependent mechanism. Owing to this promising effect, we aimed to determine in vivo activity of the cyclotide [T20K]kalata B1 using the MS mouse model experimental autoimmune encephalomyelitis (EAE). Treatment of mice with the cyclotide resulted in a significant delay and diminished symptoms of EAE by oral administration. Cyclotide application substantially impeded disease progression and did not exhibit adverse effects. Inhibition of lymphocyte proliferation and the reduction of proinflammatory cytokines, in particular IL-2, distinguish the cyclotide from other marketed drugs. Considering their stable structural topology and oral activity, cyclotides are candidates as peptide therapeutics for pharmaceutical drug development for treatment of T-cell-mediated disorders.

Idiopathic pulmonary fibrosis (IPF) is a life-threatening disease with limited treatment options. Additionally, the lack of a complete understanding of underlying immunological mechanisms underscores the importance of discovering novel options for therapeutic intervention. Since the PI3K/PTEN pathway in myeloid cells influences their effector functions, we wanted to elucidate how sustained PI3K activity induced by cell-type specific genetic deficiency of its antagonist PTEN modulates IPF, in a murine model of bleomycin-induced pulmonary fibrosis (BIPF). We found that myeloid PTEN deficient mice (PTENMyKO), after induction of BIPF, exhibit increased TGF-β1 activation, mRNA expression of pro-collagens and lysyl oxidase as well as augmented collagen deposition compared to wild-type littermates, leading to enhanced morbidity and decreased survival. Analysis of alveolar lavage and lung cell composition revealed that PTENMyKO mice exhibit reduced numbers of macrophages and T-cells in response to bleomycin, indicating an impaired recruitment function. Interestingly, we found dysregulated macrophage polarization as well as elevated expression and release of the pro-fibrotic cytokines IL-6 and TNF-α in PTENMyKO mice during BIPF. This might point to an uncontrolled wound healing response in which the inflammatory as well as tissue repair mechanisms proceed in parallel, thereby preventing resolution and at the same time promoting extensive fibrosis.

The activation of innate immune cells triggers numerous intracellular signaling pathways, which require tight control to mount an adequate immune response. The PI3K signaling pathway is intricately involved in innate immunity, and its activation dampens the expression and release of proinflammatory cytokines in myeloid cells. These signaling processes are strictly regulated by the PI3K antagonist, the lipid phosphatase, PTEN, a known tumor suppressor. Importantly, PTEN is responsible for the elevated production of cytokines such as IL-6 in response to TLR agonists, and deletion of PTEN results in diminished inflammatory responses. However, the mechanisms by which PI3K negatively regulates TLR signaling are only partially resolved. We observed that Arginase I expression and secretion were markedly induced by PTEN deletion, suggesting PTEN(-/-) macrophages were alternatively activated. This was mediated by increased expression and activation of the transcription factors C/EBPβ and STAT3. Genetic and pharmacologic experimental approaches in vitro, as well as in vivo autoimmunity models, provide convincing evidence that PI3K/PTEN-regulated extracellular Arginase I acts as a paracrine regulator of inflammation and immunity.

Zielsetzung: Das maligne Pleuramesotheliom (MPM) ist eine hoch aggressive und therapieresistente Krebserkrankung mit steigender Inzidenz bedingt durch Asbestexposition während der 2. Hälfte des 20 Jahrhunderts. Wachstumsfaktoren der Activin Superfamilie sind im malignen Wachstum von versch[for full text, please go to the a.m. URL], 20. Jahrestagung der Deutschen Gesellschaft für Thoraxchirurgie

Hintergrund: Aktivine gehören zur TGF-β Familie an Wachstumsfaktoren und spielen eine wichtige Rolle in der Embryonalentwicklung, in Entzündungsvorgängen, in Wachstum, Differenzierung und Zelltod um nur einige Funktionen zu erwähnen. Bis heute sind die Funktion und der Signaltransduktionsmechanismus von Aktivin βE, der als letztes entdeckten Untereinheit, welcher vor allem in der Leber exprimiert wird, unklar. Aktivin E ist herabreguliert im Leberzellkarzinom und überexprimiert in vielen Leukämie Zelllinien. Das Ziel dieser Studie war, den Signalmechanismus von Aktivin E in Hepatom und Leukämie Zelllinien zu untersuchen und herauszufinden, wie es zum malignen Wachstum beiträgt. Methoden: Für die Untersuchung der Funktionen von Aktivin E in malignen Zellen wurde ein Doppelansatz durchgeführt. Für die Etablierung von stabilen Klonen mit erhöhter Aktivin E Expression wurden Expressionsvektoren generiert und durch Lipofektion in Zellen mit niedrigem endogenem Aktivin E transfiziert. Gleichzeitig wurde Aktivin E mittels sh-Lentiviren in Zelllinien mit relativ hoher Aktivin E Expression hinabreguliert. Zusätzlich wurde ein Baculovirus Expressionssystem angewendet, um rekombinantes Aktivin E zu produzieren, welches bis heute noch nicht kommerziell erhältlich ist. Mittels unterschiedlicher in vitro Assays wurden stabile Klone mit Kontrollzellen verglichen und auf phänotypische Unterschiede bezüglich Proliferation, Viabilität, Adhäsions-unabhängiges Wachstum, Klonogenität und Zellzyklusphasenverteilung untersucht. Um potentielle Signalkaskaden zu detektieren, in die Aktivin E involviert ist, wurden Expressionsanalysen mit 4x44k Expressionsarrays durchgeführt. Ergebnisse: Überexpression oder verminderte Expression von Aktivin E zeigte in MTT- und Proliferationsuntersuchungen keine stimulierende oder inhibierende Wirkung auf die Proliferation oder Viabilität der jeweiligen Zelllinien. Die Verteilung der Zellzyklusphasen war ebenfalls unverändert zwischen stabilen Klonen und Kontrollzellen. Im Gegensatz dazu reduzierte eine Überexpression von Aktivin E die Proliferation im Soft Agar Assay für Adhäsions-unabhägiges Wachstum, und die Gröβe der Klone im Clonogenic Assay. In Migrationsassays hatten Aktivin E überexprimierende Zellen eine reduzierte laterale Motilität, jedoch eine erhöhte Fähigkeit durch Poren von Membranen zu wandern. Histidin-epitopmarkierte Aktivine konnten dimerisieren, aber eine Bioaktivität konnte nicht nachgewiesen werden, da das produzierte rekombinante Aktivin A keine Smad2/3 Phosphorylierung auslösen konnte. Die Expressionsanalyse zeigte, dass einige in der Apoptose involvierte Gene durch Aktivin E hochreguliert wurden, während das verwandte Zytokin Aktivin A stark herab reguliert war. Diverse andere Gene, die in verschiedene Signalkaskaden involviert sind, waren zusätzlich stark reguliert und sollten weiter untersucht werden. Schlussfolgerung: Bei Langzeitversuchen mit Aktivin E überexprimierenden Zellen werden anti-proliferative Effekte beobachtet, vor allem in in vivo ähnlichen Experimenten. Aktivin E interagiert mit vielen Signalkaskaden ohne bisher einem bestimmten Rezeptor zugeordnet werden zu können., Background: Activins belong to the extended transforming growth factor beta superfamily of cytokines which play key roles in e.g. embryonic development, inflammation, growth, differentiation and death of cells to mention just some of their functions. Until now the function and signaling mechanism of activin βE, the latest activin subunit to be discovered, which is prominently expressed in the liver, is unclear. Activin E was found downregulated in hepatocellular carcinoma and elevated in multiple leukemia cell lines. The aim of the present study was to investigate activin E signaling in hepatoma and leukemia cell models and how it could contribute to malignancies. Methods: A dual approach was conducted in order to investigate activin E functions in malignant cells. For establishment of stable clones with increased activin E level, expression vectors were generated and transfected via lipofection into cell lines with low endogenous activin E levels. At the same time a lentivirus-mediated knockdown of activin βE was performed in cell lines expressing high endogenous levels of activin E. Additionally a baculovirus expression system was used for the production of histidin-tagged activin E, because recombinant activin E is still not available commercially. Phenotypic differences between stable clones and their respective controls were examined by several in vitro assays measuring proliferation, viability, migration, anchorage independent growth, clonogenicity and cell cycle distribution. To find potential pathways activin E might be involved in, 4x44k expression arrays were carried out. Results: In MTT and proliferation assays no stimulation or inhibition of proliferation and viability were obtained when activin E levels were elevated or decreased. The cell cycle distribution did not differ between stable clones and control cells. In contrast, Activin βE reduced anchorage-indepent growth in three-dimensional soft agar assays and clone size in clonogenic assays. Migration assays revealed a slightly reduced motility in lateral migration and increased ability to pass through pores of transwell membranes when activin E levels were elevated. Baculovirus-produced Histidin-tagged activins were able to dimerize but bioactivity of the recombinant proteins could not be achieved, since the generated recombinant activin A could not activate Smad2/3 phosphorylation. The expression array revealed that several apoptosis-related genes were upregulated in activin E overexpessing cells, and the related cytokine activin A was strongly down-regulated in one of the hepatome cell lines. Several other genes involved in different signalling cascades were regulated and need further investigation. Conclusion: Long-term examination of activin E overexpressing cells reveals anti-proliferative effects, especially in in vivo like experiments. Activin E crosstalks with multiple signaling cascades but cannot be connected to a certain receptor, thus signaling mechanisms need further investigation.

Background MicroRNA (MiR)146a is a key regulator of the innate immune response and has also been shown to suppress cancer development in myeloid cells. Elevated expression of miR-146a has been detected in synovial tissue of rheumatoid arthritis patients, but its function is not clear yet. Thus the role of miR-146a in inflammatory arthritis needs to be clarified. Materials and Methods We induced K/BxN serum transfer arthritis in wild type and miR-146a -/- mice. As a second inflammatory arthritis model we crossed miR-146a deficient into hTNFtg mice. Disease severity was assessed clinically and histologically in both arthritis models. Serum cytokine levels were measured by Elisa. Results Absence of miR-146a leads to increased clinical signs of the induced serum transfer arthritis. In line, higher serum levels of the proinflammatory cytokines IL12 and TNF were measured in miR146a deficient mice compared to wt mice. When we crossed miR-146a -/- mice into hTNFtg mice, while detecting no clinical difference between hTNFtg and miR146a/hTNFtg mice, we found a significant increase in synovial inflammation. Even more striking, miR146a/hTNFtg mice displayed a more than twofold increase in local bone destruction and number of osteoclasts in the tarsal joints of the mice. Of note, in vitro osteoclast generation was reduced in miR146a -/- mice. Conclusion Data from these two arthritis models reveal a negative regulatory role of the miR-146a in inflammatory arthritis. Mice lacking miR-146a are clinically worse than their wild type counterparts with concomitant higher proinflammatory cytokine production in serum transfer arthritis. In addition, microRNA 146a has important anti-erosive properties in TNF-driven local bone destruction and osteoclastogenesis, as mice lacking this microRNA display highly increased joint destruction compared to WT. These results identify an important anti-inflammatory role of miR-146a, which might possibly be exploited for therapeutic purposes.