ITCRE is committed to helping most of the children in Tamil Nadu to fulfill their basic right to the education that will help them build a bright future. ITCRE (Indian Training Center for Rural Education ) is a volunteer non-profit organization formed by young people from various Educational background to help rural children to reach their goal by giving an opportunity to get trained by their primary education. Universal Compulsory Primary Education, with its challenges of keeping poor children in school and maintaining quality of education in rural ar eas, has been difficult to achieve. India, being a developing nation, struggles with challenges in its primary Education and strives to reach 100% literacy. Education leads to economic growth, social and political stability, declining crime rates and improved social services. Keeping children in school is important not only to the children, but to the rest of the community, and to the nation as well. In addition, some social customs deny education to girls, and children who are orphaned are almost always placed in situations that reduce their chances for education. There are many reasons for that, not the least of which is poverty itself which forces families to put children to work or into other situations because they cannot afford to keep them at home and in school. Play Arunagirinathar Thiruppugazh hit new songs.
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Education is recognized as one of the keys to fighting poverty, but despite the awareness of that fact too many children in Tamil Nadu are not in school. Arunagirinathar Thiruppugazh Songs Download- Listen to Arunagirinathar Thiruppugazh songs MP3 free online. "We are currently utilizing this information to develop novel therapeutic strategies for patients suffering from severe forms of cardiomyopathy.India has been major seat of learning for thousands of years, dating back to ancient seats of learning like Nalanda. "We can help patients learn if their RBM20 mutation will likely result in the severe form of the disease so that their physician can devise an appropriate therapy," added Professor Gotthardt. Towards utilizing these findings in a clinical setting, Professor Gotthardt has developed a technique to characterize the functional consequences of individual RBM20 mutations. Many of these genes have previously been tied to cardiomyopathy, ion-homeostasis, and sarcomere biology and future analysis will help resolve their individual contribution to the progression of the disease. Included in this group was titin, thus validating the group's previous findings. Parrish, 1 Vita Dauksaite, 3 Padmanabhan Vakeel, 3 Sabine Klaassen, 4 Brenda Gerull, 4 Ludwig Thierfelder, 4 Vera Regitz-Zagrosek, 5 Timothy A. Radke, 3 Martin Liss, 3 Thirupugal Govindarajan, 3 Henrike Maatz, 2 Herbert Schulz, 2 Shijun Li, 1 Amanda M. The researchers also identified a set of 31 genes shared by humans and rats that regulate splicing with RBM20. Wei Guo, 1, 10 Sebastian Schafer, 2, 10 Marion L.
The rats with this mutation also shared many phenotypic similarities with human patients suffering from RBM20 related cardiomyopathy specifically, ventricular enlargement, arrhythmia, increased rate of sudden death, and extensive fibrosis. Using genome-wide mapping techniques, the researchers found a loss-of-function mutation in RBM20 in all the rats that expressed the pathological titin isoform. "Titin naturally shortens around birth as the blood flow is redirected through the heart," Professor Gotthardt explained, "but these rats maintained the excessively long embryonic titin isoforms, which suggests a cause for their cardiomyopathy."
Professor Marion Greaser of the University of Wisconsin-Madison, USA, had recently identified a naturally occurring rat strain deficient in titin splicing, which resulted in an elongated titin protein. The ventricular filling of the heart is regulated by the different protein isoforms of titin which are produced through alternative splicing, a process in which the protein-coding regions of RNA (the exons) are connected in different ways, resulting in multiple mRNAs (messenger RNAs) that give rise to many proteins. Understanding this molecular mechanism behind heart function and failure, could lead to more efficient molecular diagnosis and therapies for this sometimes insidious disease.
Professor Michael Gotthardt and Professor Norbert Hübner of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany, and colleagues have found that the RNA binding motif protein 20 (RBM20), a gene previously tied to hereditary cardiomyopathy, regulates titin splicing.