170,999 research outputs found
Epigenetic-based therapies for Friedreich ataxia
This article has been made available through the Brunel Open Access Publishing Fund.Friedreich ataxia (FRDA) is a lethal autosomal recessive neurodegenerative disorder caused primarily by a homozygous GAA repeat expansion mutation within the first intron of the FXN gene, leading to inhibition of FXN transcription and thus reduced frataxin protein expression. Recent studies have shown that epigenetic marks, comprising chemical modifications of DNA and histones, are associated with FXN gene silencing. Such epigenetic marks can be reversed, making them suitable targets for epigenetic-based therapy. Furthermore, since FRDA is caused by insufficient, but functional, frataxin protein, epigenetic-based transcriptional re-activation of the FXN gene is an attractive therapeutic option. In this review we summarize our current understanding of the epigenetic basis of FXN gene silencing and we discuss current epigenetic-based FRDA therapeutic strategies. © 2014 Sandi, Sandi, Anjomani Virmouni, Al-Mahdawi and Pook
Offline to online : 75 tahun siber dan sandi mengabdi
Buku ini didedikasikan untuk memenuhi ketersediaan informasi yang valid sebagai dasar pengambilan kebijakan terkait aspek kebijakan di bidang politik, hukum dan keamanan yang dapat dipertanggungjawabkan kesahihannya. Bibliografi : halaman 225-227, indeksJakartaxxviii, 268 halaman : ilustrasi ; 24 c
APLIKASI BELAJAR SANDI MORSE UNTUK PRAMUKA
Pada penelitian ini dibuat suatu Aplikasi Belajar Sandi Morse Untuk Pramuka. Yaitu suatu aplikasi desktop atau tools yang dapat membantu siswa pramuka dalam belajar menterjemahkan sandi morse secara mudah dan praktis.
Dalam pembuatan aplikasi ini digunakan bahasa pemrograman Borland C++ Builder 5.0. Selain menggunakan bahasa pemrograman pembangunan dan perancangan aplikasi ini menggunakan pemodelan UML (Unified Modelling Language), yang menyertakan beberapa digram seperti : Use Case Diagram, Class Diagram, Sequence Diagram dan Activity Diagram.
Dengan dibuatnya Aplikasi Belajar Sandi Morse Untuk Pramuka ini diharapkan dapat membantu para siswa pramuka atau user secara umum untuk mengatasi kesulitan dalam belajar menterjemahkan sandi morse. Baik menterjemahkan dari teks ke morse serta bunyi ataupun menterjemahkan dari morse ke teks serta bunyi.
Kata kunci : Bunyi, Borland C++ Builder 5.0, Menterjemahkan, Morse, Sandi, Teks, UML
Self-supervised Antigen Detection Artificial Intelligence (SANDI)
Multiplexed pathology imaging techniques allow spatially resolved analysis of cell phenotypes for interrogating disease biology. Existing methods for cell phenotyping in multiplex images require extensive annotation workload due to the need for fully supervised training. To overcome this challenge, we develop SANDI, a self-supervised-based pipeline that learns intrinsic similarities in unlabeled cell images to mitigate the requirement for expert supervision. The capability of SANDI to efficiently classify cells with minimal manual annotations is demonstrated through the analysis of 3 different multiplexed immunohistochemistry datasets. We show that in coupled with representations learnt by SANDI from unlabeled cell images, a linear Support Vector Machine classifier trained on 10 annotations per cell type yields a higher or comparable weighted F1-score to the supervised classifier trained on an average of about 300–1000 annotations per cell type. By striking a fine balance between minimal expert guidance and the power of deep learning to learn similarity within abundant data, SANDI presents new opportunities for efficient, large-scale learning for multiplexed imaging data
Sandi Moored and Rick Fladeland
Sandi Moore, daughter of Mr. anf Mrs. Marvin Moore, and Rick Fladeland, son of Mr. and Mrs. Darrell C. Fladeland of Grand Junction, announce their marriage
Analisis Terhadap Kesaksian Polisi (Studi Kasus Putusan Mahkamah Agung Nomor 1531 K/pid.Sus/2010 / oleh Willy Sandi Subakti
abstrak (A) Nama: Willy Sandi Subakti (B) NIM : 205090124 (C) Judul Skripsi: Analisis Terhadap Kesaksian Polisi (Studi Kasus Putusan Mahkamah Agung Nomor 1531 K/pid.Sus/2010 (D) Halaman:vi + 109 + 3 Daftar pustaka + lampiran; 2013 (E) Kata Kunci:Keterangan Saksi Polisi, Ganti Rugi Putusan Bebas (F) Isi: Saksi memegang peranan penting dalam upaya pembuktian kesalahan terdakwa di depan sidang pengadilan selain dari keyakinan hakim. Saksi merupakan alat pembuktian yang paling utama dalam hukum pidana. Saksi dalam Pasal 1 angka 2 KUHAP adalah orang yang dapat memberikan keterangan guna kepentingan penyidikan, penuntutan dan peradilan tentang suatu perkara pidana yang mendengar sendiri, melihat sendiri dan mengalami sendiri. Ket San seorang yang didakwa dan diputus oleh Pengadilan Negeri Sambas (Kalimantan Barat) dan Pengadilan Tinggi Pontianak dengan Undang-Undang Psikotropika telah dinyatakan bersalah melakukan tindak pidana secara tanpa hak memiliki dan membawa psikotropika golongan I jenis ekstasi melanggar unsur pasal 59 ayat (1) UU Psikotropika secara tanpa hak memiliki, menyimpan, dan/atau membawa psikotropika golongan I. Tetapi putusan tersebut kemudian dibatalkan oleh putusan Mahkamah Agung, Ket San dinyatakan tidak bersalah dan dibebaskan dari seluruh dakwaan. Mengapa Hakim Mahkamah Agung dalam Putusan Nomor 1531 K/Pid.Sus/2010 tidak dapat menerima dan meragukan kebenaran keterangan saksi Polisi? Dan Upaya yang dapat dilakukan Ket San yang diputus tidak terbukti secara sah dan meyakinkan melakukan tindak pidana psikotropika? Dapat menuntut ganti rugi baik melalui perdata berdasarkan pasal 1365 dan pasal 95 KUHAP. Dalam penulisan ini menggunakan metode penelitian hukum normatif yang didukung dengan hasil wawancara. Kesimpulan dari hasil penelitian adalah pihak kepolisian mempunyai kepentingan terhadap perkara tidak dapat menjadi saksi di pengadilan, karena keterangannya pasti memberatkan, menyudutkan atau merekayasa. Saran bagi pemerintah gugatan ganti kerugian terhadap terdakwa yang diputus bebas dalam proses peradilan pidana tidak memberikan keadilan jika melihat pada ketentuan jumlah ganti kerugian untuk direvisi. (G) Acuan: 27 (1982-2009) (H) Pembimbing: Sugandi Ishak, S.H., M.H. (I) Penulis: Willy Sandi Subakt
Ephemeral Museums in Pandemic Era: Bari and the Museo Provinciale that Was There, that Has Been and Has Never Been
The proposal introduces the theme of the communicative resilience of exhibitions during the Pandemic Era. On March 7, 2020, Italy and its museums, as well as the countless exhibitions housed in their rooms, were closed leaving hundreds, perhaps thousands, of works without the public: from the paintings of Raphael (Rome, Scuderie del Quirinale), to the tables of the Griffoni Polyptych assembled after three hundred years (Bologna, Palazzo Fava), to the statues of Canova (Rome, Palazzo Braschi), to the Sant'Antonio by Antonio Vivarini and to the San Felice in the chair by Lorenzo Lotto chased by Bernard Berenson in his Apulian 'pilgrimages' (Bari, Palazzo Ateneo). Indeed, the latter is the exhibition to which particular attention is paid here. The spaces of the ancient Museum have come back to life with the exhibition “Il Museo che non c’è. Arte, collezionismo, gusto antiquario nel Palazzo degli Studi di Bari 1875-1928”. The exhibition involved lenders institutions such as Villa I Tatti - The Harvard University Center for Italian Renaissance Studies, the Central State Archive in Rome, the Pinacoteca of Bari 'Corrado Giaquinto' and several others. The exhibition in Bari was inaugurated on February 28th. After the first five days only the exhibition was closed for the advance of COVID 19 virus. In the 'great hall' - as the main space of the ancient Provincial Museum was called - everything remained suspended and perfectly finished: showcases, exhibitors, paintings, statues, clay and stone art objects. However, there was no longer the possibility of letting people, visitors enter. We said that it would have been wonderful to be said that it would have been wonderful to be able to reopen it at least 'virtually'. And so we did, with an immersive and advanced teaching perspective
Valutazione di produttività e misure di efficienza con applicazioni al settore del trasporto pubblico
Generation and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell models
This article has been made available through the Brunel Open Access Publishing Fund.Background: Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by GAA repeat expansion in the first intron of the FXN gene, which encodes frataxin, an essential mitochondrial protein. To further characterise the molecular abnormalities associated with FRDA pathogenesis and to hasten drug screening, the development and use of animal and cellular models is considered essential. Studies of lower organisms have already contributed to understanding FRDA disease pathology, but mammalian cells are more related to FRDA patient cells in physiological terms. Methodology/Principal Findings: We have generated fibroblast cells and neural stem cells (NSCs) from control Y47R mice (9 GAA repeats) and GAA repeat expansion YG8R mice (190+120 GAA repeats). We then differentiated the NSCs in to neurons, oligodendrocytes and astrocytes as confirmed by immunocytochemical analysis of cell specific markers. The three YG8R mouse cell types (fibroblasts, NSCs and differentiated NSCs) exhibit GAA repeat stability, together with reduced expression of frataxin and reduced aconitase activity compared to control Y47R cells. Furthermore, YG8R cells also show increased sensitivity to oxidative stress and downregulation of Pgc-1α and antioxidant gene expression levels, especially Sod2. We also analysed various DNA mismatch repair (MMR) gene expression levels and found that YG8R cells displayed significant reduction in expression of several MMR genes, which may contribute to the GAA repeat stability. Conclusions/Significance: We describe the first fibroblast and NSC models from YG8R FRDA mice and we confirm that the NSCs can be differentiated into neurons and glia. These novel FRDA mouse cell models, which exhibit a FRDA-like cellular and molecular phenotype, will be valuable resources to further study FRDA molecular pathogenesis. They will also provide very useful tools for preclinical testing of frataxin-increasing compounds for FRDA drug therapy, for gene therapy, and as a source of cells for cell therapy testing in FRDA mice. © 2014 Sandi et al
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