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MEHR ERFAHREN

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Functional characterization of the ‘PBX interacting protein’ (HPIP) in normal and malignant human haematopoiesis.

von Dr. Pawandeep Kaur

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[1.] Pak/Fragment 032 01 - Diskussion
Zuletzt bearbeitet: 2014-04-06 06:49:07 Hindemith
Ahmed 2007, Fragment, Gesichtet, KomplettPlagiat, Pak, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
SleepyHollow02
Gesichtet
Yes
Untersuchte Arbeit:
Seite: 32, Zeilen: 1-14, 17-29
Quelle: Ahmed 2007
Seite(n): 32, 33, Zeilen: 32: 7-20; 33: 3-14
[Introduction of retroviral vectors into PG13] cells results in the production of retrovirus virions capable of infecting cells from many species excluding mice.

K562: An erythroleukemia cell line derived from a chronic myeloid leukaemia patient in blast crisis. K562 cells were purchased from ATCC.

M2-10B4 j-GCSF-tkneo j-IL-3-hytk: Murine M2-10B4 fibroblasts engineered to produce high levels of both human granulocyte colony-stimulating factor (GCSF) and interleukin-3 (IL-3; 190 and 4 ng/mll, respectively), referred henceforth as M2-10B4 G-CSF / IL-3, were provided courteously provided by Connie Eaves (Terry Fox Laboratory, Vancouver, Canada).

Sl/Sl j-SF-tkneo j-IL-3-hytk: SI/SI fibroblasts engineered to produce high levels of soluble Steel factor (SF), with or without production of the transmembrane form of SF (60 and 4 ng/ ml, respectively), referred henceforth as Sl/Sl SF / IL-3, were provided kindly by Connie Eaves (Terry Fox Laboratory, Vancouver, Canada).

[• MS-5: Mouse stromal cells established by irradiation of the adherent cells in long-term bone marrow cultures derived from C3H/HeNSlc strain mice.]

3.1.4. The NOD-SCID Mice

The NOD/LtSz-scid strain was generated by crossing the SCID mutation from C.B-17- SCID mice onto the NOD background. C.B-17-scid mice lack functional T & B lymphocytes. The NOD strain mouse is an animal model of spontaneous autoimmune T-cell mediated insulin dependent diabetes mellitus (IDDM); however they have multiple defects in innate immunity. They are deficient in NK cell activity; display defects in myeloid development and function, and cannot generate either the classical or alternative pathways of haemolytic complement activation.

The NOD/LtSz-scid lacks an adaptive immune system; due to the absence of T cells, they do not develop autoimmune IDDM and remain insulitis- and diabetes free throughout life. However they carry the innate immune defects present in the parental NOD/Lt stock of mice.109


109.Lowry PA, Shultz LD, Greiner DL, et al. Improved engraftment of human cord blood stem cells in NOD/LtSz-scid/scid mice after irradiation or multiple-day injections into unirradiated recipients. Biol Blood Marrow Transplant. 1996;2:15-23.

[page 32]

Introduction of retroviral vectors into PG13 cells results in the production of retrovirus virions capable of infecting cells from many species excluding mice.

K562: An erythroleukemia cell line derived from a chronic myeloid leukemia patient in blast crisis. K562 cells were purchased from ATCC.

M2-10B4 j-GCSF-tkneo j-IL-3-hytk: Murine M2-10B4 fibroblasts engineered to produce high levels of both human granulocyte colony-stimulating factor (G-CSF) and interleukin-3 (IL-3; 190 and 4 ng/mll, respectively), referred henceforth as M2-10B4 G-CSF / IL-3, were provided courteously provided by Connie Eaves (Terry Fox Laboratory, Vancouver, Canada).

Sl/Sl j-SF-tkneo j-IL-3-hytk: SI/SI fibroblasts engineered to produce high levels of soluble Steel factor (SF), with or without production of the transmembrane form of SF (60 and 4 ng/ ml, respectively), referred henceforth as Sl/Sl SF / IL-3, were provided kindly by Connie Eaves (Terry Fox Laboratory, Vancouver, Canada).

[page 33]

3.1.6 The NOD-SCID Mice:

The NOD/LtSz-scid strain was generated by crossing the SCID mutation from C.B-17-scid mice onto the NOD background. C.B-17-scid mice lack functional T & B lymphocytes. The NOD strain mouse is an animal model of spontaneous autoimmune T-cell mediated insulin dependent diabetes mellitus (IDDM); however they have multiple defects in innate immunity. They are deficient in NK cell activity; display defects in myeloid development and function, and cannot generate either the classical or alternative pathways of haemolytic complement activation. The NOD/LtSz-scid lacks an adaptive immune system; due to the absence of T cells, they do not develop autoimmune IDDM and remain insulitis- and diabetes free throughout life. However they carry the innate immune defects present in the parental NOD/Lt stock of mice (Lowry et al., 1996).


Lowry,P.A., Shultz,L.D., Greiner,D.L., Hesselton,R.M., Kittler,E.L., Tiarks,C.Y., Rao,S.S., Reilly,J., Leif,J.H., Ramshaw,H., Stewart,F.M., and Quesenberry,P.J. (1996). Improved engraftment of human cord blood stem cells in NOD/LtSz-scid/scid mice after irradiation or multiple-day injections into unirradiated recipients. Biol. Blood Marrow Transplant. 2, 15-23.

Anmerkungen

The source is not given.

Sichter
(SleepyHollow02) Schumann



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