Aku, Saya dan Diriku

Introversi artinya “bersifat suka memendam rasa dan pikiran sendiri dan tidak mengutarakannya kepada orang lain”. Dalam tekanan sosial, seorang introvert dapat melakukan represi emosi dan ekspresi yang berlebihan dan jika tidak disalurkan secara sehat, maka dapat terjadi kecenderungan penyakit mental yang dikenal sebagai depersonalisasi. Dengan menggunakan boneka sebagai media berekspresi dan objek simbol yang mewakili sosok ideal penulis, penulis membuat boneka-boneka sebagai manifestasi atas fantasi yang tercipta dari emosi dan perasaan yang tidak tersampaikan supaya tersalurkan dengan sehat.Kemudian manifestasi ini menggantikan penulis untuk berbicara melalui sebuah cinematic poem yang menampilkan perjalanan emosi yang dialami penulis sehingga penulis dapat mengutarakan apa yang sebenarnya dirasakannya. Karya ini menyampaikan pemikiran terpendam, keinginan, fantasi, identitas seniman dan menjadi komunikasi internal dalam diri seniman untuk tetap jujur pada diri sendiri

Hematologia do Mylossoma duriventre (Serrasalmidae) da Bacia do Rio Solimões, Amazônia Central (Brasil).

Este estudo investigou os parâmetros hematológicos de Mylossoma duriventre Cuvier, 1817 da bacia do Rio Solimões, estado do Amazonas, Amazônia central, no Brasil. Variações intraespecíficas foram observadas para os parâmetros investigados, mas o hematócrito foi o parâmetro com menor variação. O número de eritrócitos mostrou correlação altamente positiva com o hematócrito. Nas extensões sanguíneas M. duriventre foram quantificados e caracterizados linfócitos, monócitos, neutrófilos, eosinófilos e leucócitos granular PASpositivo, mas houve predominância de linfócitos e neutrófilos. Tais leucócitos apresentaram características similares a de outras espécies de serrasalmídeos. Porém, foram observadas variações interespecíficas em alguns parâmetros investigados quando comparados a outros Serrasalmidae e Characidae da literatura. Este foi o primeiro estudo sobre parâmetros hematológicos de M. duriventre e os resultados obtidos poderão servir de comparação para outros estudos com esse peixe em outros ambientes

Mycolactone-dependent depletion of endothelial cell thrombomodulin is strongly associated with fibrin deposition in Buruli ulcer lesions

A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2ng/ml and as early as 8hrs after exposure. TM activates protein C by altering thrombin's substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells' ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone's effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tisischemia could contribute to the development of the tissue necrosis seen in BU lesions