A search in the REVIEW file of the MEDLNE library:
PRIONS AND SCRAPIE

Your search request has found 200 REFERENCES through Level 1

                            LEVEL 1 - 200 REFERENCES                             
1. [Human spongiform encephalopathies. Diseases caused by prions]., Humane
spongiforme encefalopatier Sygdomme forarsaget af prioner., 40 REFS, Jorn N;
Hansen D; Hansen NJ, Ugeskr Laeger 1996 Jul 8; 158 (28): 4066-72

2. The nature of the scrapie agent: the virus theory., 139 REFS, Narang H, Proc  Soc Exp Biol Med 1996 Jul; 212 (3): 208-24

3. The nature of the scrapie agent: the virus theory., 139 REFS, Narang H, Proc  Soc Exp Biol Med 1996 Jul; 212 (3): 208-24

4. [Prion-type pathologies: from scrapie to prion-related dementias. On the
borderline between veterinary and human pathology]., Patologias tipo prion.
Desde el scrapie a las demencias prion. En la encrucijada de la patologia
veterinaria y humana., 250 REFS, Domich L, Rev Neurol 1996 Jul; 24 (131):
785-802

5. The Ninth Datta Lecture. Molecular biology of transmissible spongiform
encephalopathies., 75 REFS, Weissmann C, FEBS Lett 1996 Jun 24; 389 (1): 3-11

6. [Creutzfeldt-Jakob disease -- a human prion disease]., Mb Creutzfeldt-Jakob
-- en human prionsygdom., 14 REFS, Buchwald E; Vorstrup S, Nord Med 1996 Jun;
111 (6): 180-35\

                         LEVEL 1 - 5 OF 200 REFERENCES                           
                 National Library of Medicine MEDLINE Database

TITL: The Ninth Datta Lecture. Molecular biology of transmissible spongiform
encephalopathies. 75 REFS

AUTH: Weissmann C

CITE: FEBS Lett 1996 Jun 24; 389 (1): 3-11

                 National Library of Medicine MEDLINE Database                                                                                                    ABST: The  prion,  the transmissible agent that causes spongiform
encephalopathies such as  scrapie,  bovine spongiform encephalopathy (BSE) and
Creutzfeldt-Jakob disease, is believed to be devoid of nucleic acid and
identical with PrPSc, a modified form of the normal host protein PrPC which is
encoded by the single copy gene Prnp. The 'protein only' hypothesis proposes
that PrPSc, when introduced into a normal host, causes the conversion of PrPC
into PrPSc; it therefore predicts that an animal devoid of PrPC should be
resistant to  prion  diseases. We generated homozygous Prnp(olo) ('PrP
knockout') mice and showed that, after inoculation with  prions,  they remained  free of  scrapie  for at least 2 years while wild-type controls all died within  6 months. There was no propagation of  prions  in the Prnp(olo) animals.
Surprisingly, heterozygous Prnp(ol+) mice, which express PrPC at about half the  normal level, also showed enhanced resistance to  scrapie  disease despite high  levels of infectious agent and PrPSc in the brain early on. After introduction
of murine PrP transgenes Prnp(olo) mice became highly susceptible to mouse but
not to hamster  prions,  while the insertion of Syrian hamster PrP transgenes
rendered them susceptible to hamster but to a much lesser extent to mouse
 prions.  These complementation experiments paved the way to the application of  reverse genetics. We have prepared animals transgenic for genes encoding PrP
with amino terminal deletions of various lengths and have found that PrP lacking 48 amino proximal amino acids, which comprise four of the five octa repeats of
PrP, is still biologically active. (AUTHOR)
                 National Library of Medicine MEDLINE Database                                                                                                    MJTR:  Prion  Diseases ET.     Prions  GE.    PrPC Proteins GE.    PrPSc
Proteins GE.

MNTR: Animal.    Human.    Immunity, Natural.    Mice.    Mice, Knockout.
    Prion  Diseases PP.     Prion  Diseases VE.     Prions  CL.     Prions  PY.     PrPC Proteins BI.    PrPC Proteins ME.    PrPC Proteins PY.    PrPSc Proteins BI.    PrPSc Proteins ME.    PrPSc Proteins PY.     Scrapie  ET.     Scrapie 
IM.    Support, Non-U.S. Gov't.  JOURNAL ARTICLE. REVIEW. REVIEW, TUTORIAL

RNUM: 0 ( Prions) ; 0 (PrPC Proteins); 0 (PrPSc Proteins)

GEOT: NETHERLANDS

IDEN: ISSN:  0014-5793. JOURNAL-CODE:  EUH. ENTRY-DATE:   960821.
JOURNAL-SUBSET:  M X. IM-DATE:  9610.

ACCE: 96273166


6. [Creutzfeldt-Jakob disease -- a human prion disease]., Mb Creutzfeldt-Jakob
-- en human prionsygdom., 14 REFS, Buchwald E; Vorstrup S, Nord Med 1996 Jun;
111 (6): 180-3

7. Transgenetics of prion diseases., 134 REFS, Prusiner SB, Curr Top Microbiol
Immunol 1996; 206: 275-304

8. [PSI] and [URE3] as yeast prions., 79 REFS, Wickner RB; Masison DC; Edskes HK Yeast 1995 Dec; 11 (16): 1671-85

9. Proposed link between transmissible spongiform encephalopathies of man and
animals [see comments]., 20 REFS, Diringer H, Lancet 1995 Nov 4; 346 (8984):
1208-10

10. The 'infective' process in scrapie and human spongiform encephalopathy
disease., 37 REFS, Adams DH, Med Hypotheses 1995 Aug; 45 (2): 214-8

11. On safari with PrP: prion diseases of animals., 84 REFS, Westaway D; Carlson GA; Prusiner SB, Trends Microbiol 1995 Apr; 3 (4): 141-7
                            LEVEL 1 - 200 REFERENCES                             
12. [Scrapie in sheep and transmissible encephalopathy of the mink]., La
tremblante du mouton et l'encephalopathie transmissible du vison., 84 REFS,
Brugere-Picoux J; Chatelain J, Pathol Biol (Paris) 1995 Feb; 43 (2): 81-90

13. Prion protein transgenes and the neuropathology in prion diseases., 80 REFS, DeArmond SJ; Prusiner SB, Brain Pathol 1995 Jan; 5 (1): 77-89

14. The neuropathology and epidemiology of bovine spongiform encephalopathy., 73 REFS, Wells GA; Wilesmith JW, Brain Pathol 1995 Jan; 5 (1): 91-103

15. The neuropathology and epidemiology of bovine spongiform encephalopathy
[published erratum appears in Brain Pathol 1995 Apr;5(2):200]., 73 REFS, Wells
GA; Wilesmith JW, Brain Pathol 1995 Jan; 5 (1): 91-103

16. Pathology of the transmissible spongiform encephalopathies with special
emphasis on ultrastructure., 156 REFS, Jeffrey M; Goodbrand IA; Goodsir CM,
Micron 1995; 26 (3): 277-98

17. [Electrophysiology of transmissible encephalopathies]., Electrophysiologie
des encephalopathies transmissibles., 98 REFS, Court L; Bert J, Pathol Biol
(Paris) 1995 Jan; 43 (1): 25-42