Curupira

Portuguese: Vou falar um pouco da lenda do Curupira que é um personagem da Amazônia e ela diz assim, bom, minha avó fala que a avó dela contava para ela que a lenda nos conta que o Curupira é a defensor dos animais, sendo ele um dos mais populares personagens do folclore brasileiro. Então é isso, entendeu? Só que ela continua dizendo que o Curupira gosta de sentar na sombra das mangeiras para comer os frutos. Lá fica entretido deliciando cada manga mas percebendo que está sendo observado, logo sai correndo numa velocidade tão grande que a humana não consegue acompanhar. Não adianta correr atrás de um curupira. Eu: Como o Curupira defende a floresta? Israel: O Curupira, ele defende a mata, a fauna, a flora...eh, dos predadores tipo cortadores, destruidores demais, esse negócio todo entendeu, então ele só parece para as pessoas que vao fazer mal pra floresta. Assim minha avó contava que ela viu uma vez o Curupira também em vida quando ela tinha vinte anos aquele negócio todo que ela morava no interior Urucurituba. Mas esse mesmo a história do Curupira. [Dito depois de uma segunda lenda contada na mesma mensagem] Então essas duas lendas estou contando para você. Se alguém tiver dúvida aí, pode falar para vim em Manaus, em Amazonas, e eles podem ver que é real, o encontro das águas e histórias reais e os antigos contam bem melhor que eu. Estou só te contando o que minha avó contou para mim, entendeu? English Translation: Israel: I will talk a little about the legend of the Curupira that is a person from the Amazon and the legend says this, well, my grandma said that her grandpa told her this legend and told us that the Curupira is the defender of the animals, hime being one of the most popular people in Brazilian folklore. So it is this, understand? Only that my grandma continued saying that the Curupira likes to sit in the shade of the mango trees to eat the fruits. There it stays enjoying every mango but noticing that it is being observed, right away it leaves running at a velocity so fast that humans can’t follow. It’s no use running after a curupira. Me: How does the Curupira defend the forest? Israel: The Curupira, he defends the jungle, the animals, the plants…um, from the predators like those who cut down trees, people who destroy too much, this whole kind of thing understand, so he only appears for the people who will harm the forest. Like that my grandma said that saw a Curupira once in real life when she was twenty years old that whole thing when she lived in the interior of Urucurituba. But this is the story of the Curupira. [After another legend told in the same conversation he said this] So these two legends that I’m telling you. If anyone has doubt there, you can tell them to come to Manaus, to Amazonas, and they can see that it is real, the meeting of the waters and the real stories and the elderly tell them way better than me. I’m just telling you what my grandma told to me, understand

The Importance of Personal Possessions for the Development of a Sense of Home of Nursing Home Residents

Personal possessions of nursing home residents can contribute to their sense of home. This study investigated which of the personal belongings were considered most important, and if these items indeed contributed to a sense of home. A qualitative research was conducted with 27 nursing home residents. Photographs, paintings, and pieces of furniture are objects with sentimental value. The television set is valued for its practical function. Residents of larger rooms have more flexibility in bringing along personal items, including pieces of furniture. The results of this study can be used for the design of nursing homes or for making informed choices during the process of institutionalization

Development of the rhopalial nervous system in Aurelia sp.1 (Cnidaria, Scyphozoa)

We examined the development of the nervous system in the rhopalium, a medusa-specific sensory structure, in Aurelia sp.1 (Cnidaria, Scyphozoa) using confocal microscopy. The rhopalial nervous system appears primarily ectodermal and contains neurons immunoreactive to antibodies against tyrosinated tubulin, taurine, GLWamide, and FMRFamide. The rhopalial nervous system develops in an ordered manner: the presumptive gravity-sensing organ, consisting of the lithocyst and the touch plate, differentiates first; the “marginal center,” which controls swimming activity, second; and finally, the ocelli, the presumptive photoreceptors. At least seven bilaterally arranged neuronal clusters consisting of sensory and ganglion cells and their neuronal processes became evident in the rhopalium during metamorphosis to the medusa stage. Our analysis provides an anatomical framework for future gene expression and experimental studies of development and functions of scyphozoan rhopalia

Bioavailable Trace Metals in Neurological Diseases

Medical treatment in Wilson’s disease includes chelators (d-penicillamine and trientine) or zinc salts that have to be maintain all the lifelong. This pharmacological treatment is categorised into two phases; the first being a de-coppering phase and the second a maintenance one. The best therapeutic approach remains controversial, as only a few non-controlled trials have compared these treatments. During the initial phase, progressive increase of chelators’ doses adjusted to exchangeable copper and urinary copper might help to avoid neurological deterioration. Liver transplantation is indicated in acute fulminant liver failure and decompensated cirrhosis; in cases of neurologic deterioration, it must be individually discussed. During the maintenance phase, the most important challenge is to obtain a good adherence to lifelong medical therapy. Neurodegenerative diseases that lead to a mislocalisation of iron can be caused by a culmination of localised overload (pro-oxidant siderosis) and localised deficiency (metabolic distress). A new therapeutic concept with conservative iron chelation rescues iron-overloaded neurons by scavenging labile iron and, by delivering this chelated metal to endogenous apo-transferrin, allows iron redistribution to avoid systemic loss of iron

Opposing Regulation of PROX1 by Interleukin-3 Receptor and NOTCH Directs Differential Host Cell Fate Reprogramming by Kaposi Sarcoma Herpes Virus

Lymphatic endothelial cells (LECs) are differentiated from blood vascular endothelial cells (BECs) during embryogenesis and this physiological cell fate specification is controlled by PROX1, the master regulator for lymphatic development. When Kaposi sarcoma herpes virus (KSHV) infects host cells, it activates the otherwise silenced embryonic endothelial differentiation program and reprograms their cell fates. Interestingly, previous studies demonstrated that KSHV drives BECs to acquire a partial lymphatic phenotype by upregulating PROX1 (forward reprogramming), but stimulates LECs to regain some BEC-signature genes by downregulating PROX1 (reverse reprogramming). Despite the significance of this KSHV-induced bidirectional cell fate reprogramming in KS pathogenesis, its underlying molecular mechanism remains undefined. Here, we report that IL3 receptor alpha (IL3Rα) and NOTCH play integral roles in the host cell type-specific regulation of PROX1 by KSHV. In BECs, KSHV upregulates IL3Rα and phosphorylates STAT5, which binds and activates the PROX1 promoter. In LECs, however, PROX1 was rather downregulated by KSHV-induced NOTCH signal via HEY1, which binds and represses the PROX1 promoter. Moreover, PROX1 was found to be required to maintain HEY1 expression in LECs, establishing a reciprocal regulation between PROX1 and HEY1. Upon co-activation of IL3Rα and NOTCH, PROX1 was upregulated in BECs, but downregulated in LECs. Together, our study provides the molecular mechanism underlying the cell type-specific endothelial fate reprogramming by KSHV

Kaposi's Sarcoma Associated Herpes Virus (KSHV) Induced COX-2: A Key Factor in Latency, Inflammation, Angiogenesis, Cell Survival and Invasion

Kaposi's sarcoma (KS), an enigmatic endothelial cell vascular neoplasm, is characterized by the proliferation of spindle shaped endothelial cells, inflammatory cytokines (ICs), growth factors (GFs) and angiogenic factors. KSHV is etiologically linked to KS and expresses its latent genes in KS lesion endothelial cells. Primary infection of human micro vascular endothelial cells (HMVEC-d) results in the establishment of latent infection and reprogramming of host genes, and cyclooxygenase-2 (COX-2) is one of the highly up-regulated genes. Our previous study suggested a role for COX-2 in the establishment and maintenance of KSHV latency. Here, we examined the role of COX-2 in the induction of ICs, GFs, angiogenesis and invasive events occurring during KSHV de novo infection of endothelial cells. A significant amount of COX-2 was detected in KS tissue sections. Telomerase-immortalized human umbilical vein endothelial cells supporting KSHV stable latency (TIVE-LTC) expressed elevated levels of functional COX-2 and microsomal PGE2 synthase (m-PGES), and secreted the predominant eicosanoid inflammatory metabolite PGE2. Infected HMVEC-d and TIVE-LTC cells secreted a variety of ICs, GFs, angiogenic factors and matrix metalloproteinases (MMPs), which were significantly abrogated by COX-2 inhibition either by chemical inhibitors or by siRNA. The ability of these factors to induce tube formation of uninfected endothelial cells was also inhibited. PGE2, secreted early during KSHV infection, profoundly increased the adhesion of uninfected endothelial cells to fibronectin by activating the small G protein Rac1. COX-2 inhibition considerably reduced KSHV latent ORF73 gene expression and survival of TIVE-LTC cells. Collectively, these studies underscore the pivotal role of KSHV induced COX-2/PGE2 in creating KS lesion like microenvironment during de novo infection. Since COX-2 plays multiple roles in KSHV latent gene expression, which themselves are powerful mediators of cytokine induction, anti-apoptosis, cell survival and viral genome maintainence, effective inhibition of COX-2 via well-characterized clinically approved COX-2 inhibitors could potentially be used in treatment to control latent KSHV infection and ameliorate KS

Mitochondrial superclusters influence age of onset of Parkinson’s disease in a gender specific manner in the Cypriot population: A case-control study

Despite evidence supporting an involvement of mitochondrial dysfunction in the pathogenesis of some neurodegenerative disorders, there are inconsistent findings concerning mitochondrial haplogroups and their association to neurodegenerative disorders, including idiopathic Parkinson's disease (PD).To test this hypothesis for the Greek-Cypriot population, a cohort of 230 PD patients and 457 healthy matched controls were recruited. Mitochondrial haplogroup distributions for cases and controls were determined. Association tests were carried out between mitochondrial haplogroups and PD.Mitochondrial haplogroup U was associated with a reduced PD risk in the Cypriot population. After pooling mitochondrial haplogroups together into haplogroup clusters and superclusters, association tests demonstrated a significantly protective effect of mitochondrial haplogroup cluster N (xR) and supercluster LMN for PD risk only in females. In addition, for female PD cases belonging to UKJT and R (xH, xUKJT) haplogroup, the odds of having a later age of onset of PD were 13 and 15 times respectively higher than the odds for female cases with an H haplogroup.Statistically significant associations regarding PD risk and PD age of onset were mostly detected for females thus suggesting that gender is a risk modifier between mitochondrial haplogroups and PD status / PD age of onset. The biological mechanisms behind this gender specificity remain to be determined