Hasil Pencarian  ::  Simpan CSV :: Kembali

Hasil Pencarian

Ditemukan 3 dokumen yang sesuai dengan query
cover
Resmi Kartini Setiawan
Amiloidosis pada hati dan limpa mencit C3H yang diinduksi C. Albicans dan Kasein = Amyloidosis of the liver and spleen of C3H mice induced by C. Albicans and Casein
" ABSTRAK Ruang Lingkup dan Cara Penelitian: Amiloid merupakan suatu substansi protein patologis. Amiloidosis pada manusia merupakan penyakit dengan kelainan klinik yang sangat bervariasi, maka penyelidikan amiloidosis pada hewan percobaan mempunyai arti yang penting. Dinding sel C. albicans mengandung mannan, yang diduga berperan dalam terjadinya amiloidosis; demikian pula kasein dikenal dapat menimbulkan amiloidosis pada hewan percobaan. Perjajanan penyakit atau proses terjadinya amiloidosis pada kedua cara induksi tersebut belum jelas. Tujuan penelitian ini adalah mempelajari proses terjadinya amiloidosis ... "
Jakarta: Fakultas Kedokteran Universitas Indonesia, 1986
T-Pdf
UI - Tesis Membership  Universitas Indonesia Library
cover
Simatupang, Lydia D.
Chronic diarrhea due to intestinal amyloidosis
" Amyloidosis is a rare disease, when diagnosed it's incurable and mostly affect over 40 years old male. Diagnostic is confirmed if histopathologic stained positive with Congo red and evidence of monoclonal protein. Survivals for untreated patients are 13 months in primary amyloidosis but if secondary to other chronic disease and systemic, survival could be 3-4 years. It can not be prevented but when affected, control of the underlying illness can prevent progression of amyloidosis. We report ... "
The Indonesia Journal of Gastroenterology Hepatology and Digestive Endoscopy, 2005
IJGH-6-3-Des2005-92
Artikel Jurnal  Universitas Indonesia Library
cover
Farid Rahimi, editor
Non-fibrillar amyloidogenic protein assemblies— Common cytotoxins underlying degenerative diseases
" Amyloid-forming proteins are implicated in over 30 human diseases. The proteins involved in each disease have unrelated sequences and dissimilar native structures, but they all undergo conformational alterations to form fibrillar polymers. The fibrillar assemblies accumulate progressively into disease-specific lesions in vivo. Substantial evidence suggests these lesions are the end state of aberrant protein folding whereas the actual disease-causing culprits likely are soluble, non-fibrillar assemblies preceding the aggregates. The non-fibrillar protein assemblies range from small, ... "
Dordrecht: [, Springer], 2012
e20417827
eBooks  Universitas Indonesia Library