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The effects of somatostatin on spreading depression in rat neocortical tissues

von Dr. Cornelia Larissa Granz

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Statistik und Sichtungsnachweis dieser Seite findet sich am Artikelende
[1.] Clg/Fragment 024 03 - Diskussion
Zuletzt bearbeitet: 2014-05-11 22:33:39 Schumann
Clg, Fragment, Gesichtet, Matharu et al 2004, SMWFragment, Schutzlevel sysop, Verschleierung

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Verschleierung
Bearbeiter
Hindemith
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Untersuchte Arbeit:
Seite: 24, Zeilen: 3-8
Quelle: Matharu et al 2004
Seite(n): 489, 491, Zeilen: 489: l.col: 10-14; 491: r.col: 31-36
Somatostatin has been shown to block the release of numerous vasoactive peptides, including Calcitonin Gene-Related Peptide and vasoactive intestinal polypeptide e et al.(Fassler et al., 1990; Helyes, 2001). Neurons containing somatostatin are found in the regions of the central and peripheral nervous system involved in nociception, such as peripheral sensory fibres, dorsal horn of the spinal cord, trigeminal nucleus caudalis, periaqueductal gray and the hypothalamus (Schindler et al., 1997).

Fassler JE, O'Dorisio TM, Mekhjian HS, Gaginella TS (1990) Octreotide inhibits increases in shortcircuit current induced in rat colon by VIP, substance P, serotonin and aminophylline. Regul Pept 29(2-3):189-97.

Helyes Z, Pintér E, Németh J, Kéri G, Thán M, Oroszi G, Horváth A, Szolcsányi J (2001) Antiinflammatory effect of synthetic somatostatin analogues in the rat. Br J Pharmacol 134 (7):1571-9.

Schindler M, Sellers LA, Humphrey PP, Emson PC (1997)Immunohistochemical localization of the somatostatin SST2(A) receptor in the rat brain and spinal cord. Neuroscience. 76(1):225-40.

Somatostatin, an endogenously occurring 14–amino acid peptide, has been shown to inhibit the release of numerous vasoactive peptides, including CGRP19 and VIP.20

[page 491]

Neurons containing somatostatin are found in the regions of the central and peripheral nervous system involved in nociception, such as peripheral sensory fibers, dorsal horn of the spinal cord, trigeminal nucleus caudalis, periaqueductal gray, and the hypothalamus.31,32


19. Helyes Z, Pinter E, Nemeth J, et al. Anti-inflammatory effect of synthetic somatostatin analogues in the rat. Br J Pharmacol 2001;134:1571–1579.

20. Fassler JE, O’Dorisio TM, Mekhjian HS, Gaginella TS. Octreotide inhibits increases in short-circuit current induced in rat colon by VIP, substance P, serotonin and aminophylline. Regul Pept 1990;29:189 –197.

31. Krisch B. Hypothalamic and extrahypothalamic distribution of somatostatin-immunoreactive elements in the rat brain. Cell Tissue Res 1978;195:499 –513.

32. Schindler M, Holloway S, Hathway G, et al. Identification of somatostatin sst2(a) receptor expressing neurones in central regions involved in nociception. Brain Res 1998;798:25–35.

Anmerkungen

Also the passages after the here documented passage can be found in the source, but the match seems to be somewhat better with another paper by the same author, see Clg/Fragment_024_08.

The source is given further down at the end of the paragraph but without indication that the whole paragraph is taken from it including several references to the literature.

Sichter
(Hindemith) Schumann

[2.] Clg/Fragment 024 08 - Diskussion
Zuletzt bearbeitet: 2014-05-11 16:02:47 Schumann
Clg, Fragment, Gesichtet, Matharu et al 2003, SMWFragment, Schutzlevel sysop, Verschleierung

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Hood
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Untersuchte Arbeit:
Seite: 24, Zeilen: 8-15
Quelle: Matharu et al 2003
Seite(n): 12, Zeilen: l. col. 26-41
Intravenous somatostatin (25 μg/min for 20 min) was compared with treatment with ergotamine (250 μg intramuscularly), or placebo in a double-blind trial comprising 72 attacks in eight patients (Sicuteri et al., 1984). Infusion of somatostatin reduced the maximal pain intensity and the duration of pain to a level comparable with intramuscular ergotamine. In a randomized, double-blind study subcutaneous somatostatin was compared with ergotamine (Geppetti et al., 1985). Five patients were treated for three attacks by each of the drugs. Subcutaneous somatostatin and ergotamine were equally beneficial as regards effects on maximal pain intensity and the pain area, but somatostatin was less effective in reduction of the duration of headache.

Sicuteri F, Geppetti P, Marabini S, Lembeck F (1984) Pain relief by somatostatin in attacks of cluster headache. Pain 18(4):359-65.

Intravenous somatostatin 25 μg/min for 20 minutes was compared with ergotamine 250μg intramuscularly or placebo in a double-blind trial comprising 72 attacks in eight patients. [102] Infusion of somatostatin reduced the maximal pain intensity and the duration of pain significantly compared with placebo, and to a degree comparable to intramuscular ergotamine.

In another randomised, double-blind study, subcutaneous somatostatin was compared with ergotamine. [102] Five patients were treated for three attacks by each of the drugs. Subcutaneous somatostatin and ergotamine were equally beneficial as regards effects on maximal pain intensity and the pain area, but somatostatin was less effective in reducing the duration of pain.


[102] Sicuteri F. Geppetti P, Marabini S, et al. Pain relief by somatostatin in attacks of cluster headache. Pain 1984; 18: 359-65

[103] Geppetti P, Brocchi A, Caleri D, et al. Somatostatin for cluster beadache attack. In: Pfaffenrath V, Lundberg PO, Sjaastad O, editors. Updating in headache. Berlin: Spring-Verlag, 1985: 302-5

Anmerkungen

The source named "Geppetti et al., 1985" is missing in the chapter "VI. References".

Different spelling: "randomized" instead of "randomised" – a hint that the text also could have been taken from another source.

Sichter
(Hood) Schumann

[3.] Clg/Fragment 024 19 - Diskussion
Zuletzt bearbeitet: 2014-05-11 16:12:25 Schumann
BauernOpfer, Cervia et al 2008, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop

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Untersuchte Arbeit:
Seite: 24, Zeilen: 19-24
Quelle: Cervia et al 2008
Seite(n): 2224, Zeilen: l.col: 16-20, 24-30
The primary cause of neuronal death in retinal diseases is ischaemia, a condition that can be considered a final common pathway for injury in different retinal pathologies (Quigley et al., 1995; Levin and Louhab 1996). The peptide somatostatin plays important physiological roles, mostly inhibitory, which have formed the basis for the clinical use of SRIF compounds (Weckbecker et al., 2003; Cervia and Bagnoli 2007), and it may protect the retina against ischaemia in a variety of retinal diseases (Cervia et al., 2008).

[...]

Cervia D, Martini D, Ristori C, Catalani E, Timperio AM, Bagnoli P, Casini G (2008) Modulation of the neuronal response to ischaemia by somatostatin analogues in wild-type and knock-out mouse retinas. J Neurochem 106(5):2224-35.

The primary cause of neuronal death in retinal diseases is ischaemia, a condition that can be considered a final common pathway for injury in different retinal pathologies (Quigley et al. 1985, 1995; Levin and Louhab 1996; Osborne et al. 1999, 2004; Barber 2003). [...] The peptide somatostatin (somatotropin release-inhibiting factor, SRIF) plays important physiological roles, mostly inhibitory, which have formed the basis for the clinical use of SRIF compounds (Weckbecker et al. 2003; Cervia and Bagnoli 2007), and it may protect the retina against ischaemia in a variety of retinal diseases (Cervia et al. 2008).

[...]

Cervia D., Casini G. and Bagnoli P. (2008) Physiology and pathology of somatostatin in the mammalian retina: a current view. Mol. Cell. Endocrinol. 286, 112–122.

Anmerkungen

The source is given in the end for the statement "and it may protect the retina against ischaemia in a variety of retinal diseases". It is not clear to the reader that more is taken from the source including references to the literature.

Note that the reference "Cervia et al. 2008" given in the source refers to a different paper than the reference in the dissertation that has been given at the same place.

Sichter
(Hindemith) Schumann

[4.] Clg/Fragment 024 24 - Diskussion
Zuletzt bearbeitet: 2014-05-10 22:34:59 Hindemith
BauernOpfer, Clg, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Stumm et al 2004

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Graf Isolan
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Untersuchte Arbeit:
Seite: 24, Zeilen: 24-32
Quelle: Stumm et al 2004
Seite(n): 11404, 11413, Zeilen: 11404:left col. 8-11 - right col. 1-5; 11413:right col. 36-42
In non-neuronal cells, somatostatin has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by somatostatin receptors. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that somatostatin may influence neurodegeneration after brain ischemia. Activation and upregulation of somatostatin receptors type 2 in perifocal pyramidal neurons after focal ischemia were reported. Upregulation of these receptors is most likely the result of both somatostatin-derived and heterologous signals and may counteract somatostatin desensitization. Excessive activation of somatostatin receptors type 2 [in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in somatostatin receptors type 2 -deficient mice (Stumm et al., 2004).] [Page 11404]

Introduction

[...] In non-neuronal cells, SSTR2 has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by SSTRs. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion (MCAO) affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that SSTRs may influence neurodegeneration after brain ischemia.

[Page 11413]

Conclusion

Together, this study provides the first evidence for activation and upregulation of SSTR2 in perifocal pyramidal neurons after focal ischemia. Upregulation of SSTR2 is most likely the result of both SSTR2-derived and heterologous signals and may counteract SSTR2 desensitization. Excessive activation of SSTR2 in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in SSTR2-deficient mice.

Anmerkungen

The source is mentioned in the end as one of several sources mentioned in this passage. This does not make clear that the whole passage is taken from the source and that some quotations are literal.

Sichter
(Graf Isolan), Hindemith


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