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6 ungesichtete Fragmente: "verdächtig" oder "Keine Wertung"

[1.] Mag/Fragment 019 01 - Diskussion
Bearbeitet: 16. March 2014, 22:39 (Hindemith)
Erstellt: 4. March 2014, 22:25 Graf Isolan
Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel sysop, Wright 2005, ZuSichten

Typus
KeineWertung
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 19, Zeilen: 1-3
Quelle: Wright 2005
Seite(n): 59, 60, Zeilen: 59:right col. 50-54; 60: figure 2
The collectins are assembled as trimeric subunits, which multimerize to varying degrees. SP-A is mainly an octadecamer and forms a bouquet-like structure that is similar to MBL, whereas SP-D forms a dodecamer (Wright, 2005).

19a diss Mag.png

Figure 3: Collectin and C1q structure. Surfactant protein A (SP-A) and SP-D are members of a family of proteins known as collectins. a Collectins have collagen-like amino (N)-terminal regions and C-type (calcium dependent) carbohydrate-recognition domains (CRDs). Collectins consist of structural subunits that are composed of trimeric polypeptide chains, which are identical except for human SP-A. The trimers are assembled into oligomers. b SP-A and mannose-binding lectin (MBL) are octadecamers (18-mers), consisting of six trimeric subunits. SP-D is a dodecamer (12-mer), consisting of four trimeric subunits. Although C1q is structurally homologous to SP-A and MBL, it is not a collectin as it does not have a lectin domain (CRD) (adapted from Wright, 2005).


Wright JR. Immunoregulatory functions of surfactant proteins. Nat Rev Immunol. 2005 Jan; 5 (1): 58-68. Review.

[Page 59]

The collectins are assembled as trimeric subunits, which multimerize to varying degrees. SP-A is mainly an octadecamer and forms a bouquet-like structure that is similar to MBL, whereas SP-D forms a dodecamer (FIG. 2).

[Page 60]

19a source Mag.png

Figure 2 Collectin and C1q structure. Surfactant protein A (SP-A) and SP-D are members of a family of proteins known as collectins. a Collectins have collagen-like amino (N)-terminal regions and C-type (calcium dependent) carbohydrate-recognition domains (CRDs). Collectins consist of structural subunits that are composed of trimeric polypeptide chains, which are identical except for human SP-A. The trimers are assembled into oligomers. b SP-A and mannose-binding lectin (MBL) are octadecamers (18-mers), consisting of six trimeric subunits. SP-D is a dodecamer (12-mer), consisting of four trimeric subunits. Although C1q is structurally homologous to SP-A and MBL, it is not a collectin as it does not have a lectin domain (CRD). Note that these models are not drawn to scale.

Anmerkungen

The source is mentioned. Nevertheless there is no hint that the texts are identical.

The figure has not been "adapted" but rather "copied".

Sichter
(Graf Isolan)

[2.] Mag/Fragment 013 01 - Diskussion
Bearbeitet: 10. March 2014, 11:39 (Graf Isolan)
Erstellt: 5. March 2014, 08:50 Hindemith
Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel, Wright 2005, ZuSichten

Typus
KeineWertung
Bearbeiter
Hindemith
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 13, Zeilen: 1-1
Quelle: Wright 2005
Seite(n): 59, Zeilen: figure
12a diss Mag.png

Figure 2: Schematic structure of airway and alveolus and their host-defence mechanisms. The lung is constantly challenged by inhaled pathogens, pollutans [sic] and particles. Several different defence mechanisms contribute to lung defence. These include filtration in the naso-oropharynx and conducting airways, sneezing, coughing and mucociliary clearance. Small particles might reach the alveolar gas-exchange regions of the lung. Host-defence functions in the peripheral air-spaces include surfactant, other opsonins (such as immunoglobulins) and innate immune cells (including alveolar macrophages and neutrophiles [sic]). Surfactant protein A (SP-A); surfactant protein D (SP-D) (adapted from Wright, 2005).


Wright JR. Immunoregulatory functions of surfactant proteins. Nat Rev Immunol. 2005 Jan; 5 (1): 58-68. Review.

12a source Mag.png

Figure 1 Lung host-defence mechanisms. The lung is constantly challenged by inhaled pathogens, pollutants and particles. Several different defence mechanisms contribute to lung defence. These include filtration in the naso-oropharynx and conducting airways, sneezing, coughing and mucociliary clearance. Small particles might reach the alveolar gas-exchange regions of the lung. Host-defence functions in the peripheral air-spaces include surfactant, other opsonins (such as immunoglobulins) and innate immune cells (including alveolar macrophages and neutrophils). SP-A, surfactant protein A; SP-D, surfactant protein D.

Anmerkungen

The source is given, but it does not make clear that the extensive figure caption is copied literally from the source.

Neither does the word "adapted" suggest that the figure is an exact copy of the figure in the source.

Sichter
(Hindemith)

[3.] Mag/Fragment 026 05 - Diskussion
Bearbeitet: 10. March 2014, 11:52 (Graf Isolan)
Erstellt: 5. March 2014, 09:08 Hindemith
Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel, Skapenko et al 2005, ZuSichten

Typus
KeineWertung
Bearbeiter
Hindemith
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 26, Zeilen: 5-19
Quelle: Skapenko et al 2005
Seite(n): S5, Zeilen: figure
26a diss Mag.png

Figure 5: Schematic representation of T cell development. T cells originate from the common lymphoid progenitor cells in the bone marrow. They migrate as immature precursor T cells via bloodstream into thymus, which they populate as thymocytes. The thymocytes go through a series of maturation steps including distinct changes in the expression of cell surface receptors, such as the CD3 signalling complex (not shown) and the coreceptors CD4 and CD8, as well as the arrangement of their antigen receptor (T cell receptor, TCR) genes. More than 98% of the thymocytes die during maturation by apoptosis (†), as they undergo positive selection for their TCR´s compatibility with self-major histocompatibility molecules, and negative selection against those T cells that express TCRs reactive to autoantigenic peptides. In humans, the vast majority of peripheral blood T cells express TCRs consisting of α and β chains (αβ T cells). A small group of peripheral T cells bear an alternative TCR composed of γ and δ chains (γδ T cells). αβ and γδ T cells diverge early in T cell development. Whereas αβ T cells are responsible for the classical helper or cytotoxic T cell response, the function of the γδ T cells within the immune system is largely unknown. αβ T cells that survive thymic selection lose expression of either CD4 or CD8, increase the level of expression of the TCR, and leave the thymus to form the peripheral T cell repertoire (adapted from Skapenko et al., 2005).


Skapenko A, Leipe J, Lipsky PE, Schulze-Koops H. The role of the T cell in autoimmune inflammation. Arthritis Res Ther. 2005; 7 Suppl 2: S4-14. Epub 2005 Mar 16.

26a source Mag.png

Schematic representation of T cell development. T cells originate from the common lymphoid progenitor cells in the bone marrow. They migrate as immature precursor T cells via the bloodstream into the thymus, which they populate as thymocytes. The thymocytes go through a series of maturation steps including distinct changes in the expression of cell surface receptors, such as the CD3 signaling complex (not shown) and the coreceptors CD4 and CD8, and the rearrangement of their antigen receptor (T cell receptor, TCR) genes. More than 98% of the thymocytes die during maturation by apoptosis (†), as they undergo positive selection for their TCR's compatibility with self-major histocompatibility molecules, and negative selection against those T cells that express TCRs reactive to autoantigenic peptides. In humans, the vast majority of peripheral blood T cells expresses TCRs consisting of α and β chains (αβ T cells). A small group of peripheral T cells bears an alternative TCR composed of γ and δ chains (γ/δ T cells). αβ and γδ T cells diverge early in T cell development. Whereas αβ T cells are responsible for the classical helper or cytotoxic T cell responses, the function of the γδ T cells within the immune system is largely unknown. αβ T cells that survive thymic selection lose expression of either CD4 or CD8, increase the level of expression of the TCR, and leave the thymus to form the peripheral T cell repertoire.

Anmerkungen

The source is given, but it is not clear to the reader that the very extensive caption is taken from it more or less literally.

Sichter
(Hindemith)

[4.] Mag/Fragment 023 01 - Diskussion
Bearbeitet: 10. March 2014, 11:46 (Graf Isolan)
Erstellt: 5. March 2014, 13:39 Hindemith
Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel, Wright 2005, ZuSichten

Typus
KeineWertung
Bearbeiter
Hindemith
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 23, Zeilen: 1-7
Quelle: Wright 2005
Seite(n): 63, Zeilen: figure
23a diss Mag.png

Figure 4: Collectin receptors. Surfactant protein A (SP-A) and SP-D potentially bind several receptors, including SP-R210, Toll-like receptor 2 (TLR2), TLR4, signal-inhibitory regulatory protein-α (SIRP-α) and CD91-calreticulin. SP-A binds SIRP-α and inhibits production of inflammatory mediators. In contrast, when SP-A is bound to a pathogen or cellular debris, its collagen-like region is bound to CD91-calreticulin and induces inflammatory-mediator production. Nuclear factor κB, (NF-κB); protein kinase C (PKC); SRC homology 2 (SH2)-domain-containing protein tyrosine phosphatase 1 (SHP1) (adapted from Wright, 2005).


Wright JR. Immunoregulatory functions of surfactant proteins. Nat Rev Immunol. 2005 Jan; 5 (1): 58-68. Review.

23a source Mag.png

Figure 4 Collectin receptors. Surfactant protein A (SP-A) and SP-D potentially bind several receptors, including SP-R210, Toll-like receptor 2 (TLR2), TLR4, signal-inhibitory regulatory protein-α (SIRP-α) and CD91-calreticulin. SP-A binds SIRP-α and inhibits production of inflammatory mediators. By contrast, when SP-A is bound to a pathogen or cellular debris, its collagen-like region is bound to CD91-calreticulin and induces inflammatory-mediator production. NF-κB, nuclear factor-κB; PKC, protein kinase C; SHP1, SRC homology 2 (SH2)-domain-containing protein tyrosine phosphatase 1.

Anmerkungen

The source is given, but it is not clear to the reader that the extensive figure caption is taken literally from it. Neither is it clear that "adapted from" actually means "copied from".

Sichter
(Hindemith)

[5.] Mag/Fragment 110 01 - Diskussion
Bearbeitet: 10. March 2014, 11:52 (Graf Isolan)
Erstellt: 5. March 2014, 22:09 Hindemith
Bruder et al 2004, Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel, ZuSichten

Typus
KeineWertung
Bearbeiter
Hindemith
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 110, Zeilen: 1-17
Quelle: Bruder et al 2004
Seite(n): 628, 629, Zeilen: 628: r.col: last lines; 629: l.col: 1ff
1.11 DNA microarray hybridization and analysis

Total RNA from sorted AECII was isolated using the RNAeasy kit (Qiagen, Hilden, Germany). Quality and integrity of total RNA isolated from 2 x 105 sorted AECII cells was assessed by running all samples on an Agilent Technologies 2100 Bioanalyser (Agilent Technologies, Waldbronn, Germany). For RNA amplification the first round was done according to Affymetrix without biotinylated nucleotides using the Promega P1300 RiboMax Kit (Promega, Mannheim, Germany) for T7 amplification. For the second round of amplification the precipitated and purified RNA was converted to cDNA primed with random hexamers (Pharmacia, Freiburg, Germany). Second strand synthesis and probe amplification were done as in the first round with two exceptions: incubation with RNAse H preceeded the first strand synthesis to digest the aRNA, and the T7T23V oligo for initiation of the second strand synthesis was used. 12.5μg biotinylated cRNA preparation was fragmented and placed in a hybridization cocktail containing four biotinylated hybridization controls (BioB, BioC, BioD, and Cre) as recommended by the manufacturer. Samples were hybridized to an identical lot of Affymetrix MG-U74Av2 chips for 16 hours. After hybridization, GeneChips were washed, stained with streptavidin-PE and read using an Affymetrix GeneChip fluidic station scanner.

3.8 DNA microarray hybridization and analysis

The quality and integrity of the total RNA isolated from 5 x 104 cells was controlled by running all samples on an Agilent

[page 629]

Technologies 2100 Bioanalyzer (Agilent Technologies, Waldbronn, Germany). For RNA-amplification, the first round was done according to Affymetrix without biotinylated nucleotides using the Promega P1300 RiboMax Kit (Promega, Mannheim, Germany) for T7 amplification. For the second round of amplification the precipitated and cleaned aRNA was converted to cDNA using random hexamers (Pharmacia, Freiburg, Germany). Second-strand synthesis and probe amplification was done like in the first round, except for an incubation with RNAse H before first-strand synthesis to digest the aRNA and for the use of the T7T23V oligo for initiation of the synthesis of the second strand. The concentration of biotin-labeled cRNA was determined by UV absorbance. In all cases, 12.5μg of each biotinylated cRNA preparation was fragmented and placed in a hybridization cocktail containing four biotinylated hybridization controls (BioB, BioC, BioD, and Cre) as recommended by the manufacturer. Samples were hybridized to an identical lot of Affymetrix MOE430A for 16 h. After hybridization the GeneChips were washed, stained with SA–PE and read using an Affymetrix GeneChip fluidic station and scanner.

Anmerkungen

Its just the description of material and methods, but the text is largely identical and the source is not given.

Sichter
(Hindemith)

[6.] Mag/Fragment 086 21 - Diskussion
Bearbeitet: 10. March 2014, 11:53 (Graf Isolan)
Erstellt: 5. March 2014, 22:30 Hindemith
Enelow 1998, Fragment, KeineWertung, Mag, SMWFragment, Schutzlevel, ZuSichten

Typus
KeineWertung
Bearbeiter
Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 86, Zeilen: 21-22
Quelle: Enelow 1998
Seite(n): 1653, Zeilen: l.col: 31-33
A significant number of lung diseases are presumed to be T cell mediated based in part on the observation of T cell accumulation in sites of disease activity. A significant number of lung diseases are presumed to be T cell mediated based in part on the observation of T cell accumulation in sites of disease activity.
Anmerkungen

Identical text, but no source given.

Sichter
(Hindemith)

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