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| 2. |
- Lange, D, et al.
(författare)
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Autocrine endothelial regulation in brain stem vessels of newborn piglets.
- 1999
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Ingår i: Histology and histopathology. - 0213-3911. ; 14:3, s. 821-5
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Tidskriftsartikel (refereegranskat)abstract
- Vasoactive intestinal peptide (VIP) is known as a potent regulator for the development of the central nervous system (CNS). The neonatal period of brain development is characterised by rapid cellular proliferation in parallel with neuronal differentiation and angiogenesis. We examined the expression of native VIP and the VIP receptor-associated protein by immunohistochemistry as well as the expression of VIP mRNA by in situ hybridisation in the brain stem of newborn piglets. We found both the mRNA and the protein of VIP as well as the VIP receptor-associated protein in endothelial cells of veins, arteries and capillaries in the marginal zone of brain stem tissue sections, especially in pons and mesencephalon, as well as in pial vessels. The coexpression of native VIP, VIP mRNA and the VIP receptor-associated protein within the endothelium suggests the presence of an autocrine loop, which has been detected so far only in neuroblastoma cells. This expression pattern gives evidence to the immaturity of endothelial cells at birth and the presence of an adaptive response in the VIP-regulated system during the change from intra- to extrauterine life.
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| 3. |
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| 4. |
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| 5. |
- Qian, Bi-Feng, et al.
(författare)
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Changes in intestinal endocrine cells in the mouse after unilateral cervical vagotomy
- 1999
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Ingår i: Histology and Histopathology. - 0213-3911 .- 1699-5848. ; 14:2, s. 453-460
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Tidskriftsartikel (refereegranskat)abstract
- The effect of right or left unilateral cervical vagotomy on the intestinal endocrine cells was studied in 23 mice at 2 and 8 weeks after operation, respectively. The results were compared with that from 10 sham operated mice. Various types of endocrine cells in duodenum and proximal colon were detected by immunohistochemistry and quantified by computerized image analysis. In mouse duodenum, chromogranin-, CCK/gastrin-, GIP- and somatostatin-cells were significantly decreased at 2 weeks after right vagotomy, but returned to the control levels at 8 weeks. Serotonin-cells were reduced at both 2 and 8 weeks after right vagotomy. The amount of the duodenal endocrine cells did not change after left vagotomy with the exception of secretin-cells, which were diminished at 8 weeks after both right and left vagotomy. In the proximal colon, chromogranin-cells were also decreased at 2 weeks after right vagotomy. Serotonin-cells were reduced at 8 weeks after left vagotomy but not right vagotomy. There was no significant difference between the unilaterally vagotomized and the sham operated mice with regard to PYY- and glucagon-cells. It was concluded that vagotomy affected the intestinal endocrine cells in mouse. The influence was more pronounced in the small intestine than the proximal colon. The right vagus nerves seemed to exert more effect on the intestinal endocrine cells than the left ones.
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| 6. |
- Qian, Bi-Feng, et al.
(författare)
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Effects of unilateral cervical vagotomy on antral endocrine cells in mouse
- 1999
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Ingår i: Histology and Histopathology. - 0213-3911 .- 1699-5848. ; 14:3, s. 705-709
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Tidskriftsartikel (refereegranskat)abstract
- The present study was carried out to investigate the effect of unilateral cervical vagotomy on the antral endocrine cells in mouse. Fifty-four mice were randomly divided into three groups, 18 in each, for left or right cervical vagotomy, or sham operation as controls. The animals were sacrificed 2, 4, and 8 weeks after the operation, respectively. Chromogranin-, gastrin/CCK-, serotonin-, and somatostatin-cells were detected by immunohistochemistry and quantitated by computerised image analysis. The results showed that the number of chromogranin-cells was decreased in both left and right vagotomized mice after 4 weeks and remained at the same level after 8 weeks. The numbers of gastrin-, serotonin- and somatostatin-cells did not change after right vagotomy. However, the numbers of gastrin- and somatostatin-cells were decreased after left vagotomy, whereas no change was found in serotonin-cells. Endocrine cells with vacuolated cytoplasm and pyknotic nuclei were also observed during the course of time. The alteration in the antral endocrine cells observed in this study seemed to be dynamic and depended on the observation time after the operation as well as the denervated branches of the vagus nerve. This may explain, at least partially the contradictory results obtained earlier by different investigators.
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| 7. |
- Smits, Anja, et al.
(författare)
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Platelet-derived growth factor in primary brain tumors of neuroglial origin
- 1998
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Ingår i: Histology and Histopathology. - 0213-3911 .- 1699-5848. ; 13:2, s. 511-520
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Tidskriftsartikel (refereegranskat)abstract
- It has become clear that disruptions in the genome of somatic cells play a causative role in tumour development. We know that the ultimate formation of a malignancy is the result of a multistep process in which the functional loss and/or the altered or increased expression of genes play important roles. One such family of genes are the oncogenes, encoding protein products with mainly growth stimulating effects. Platelet-derived growth factor (PDGF) belongs to the family of oncogenes. It is likely that PDGF plays an essential role in the development of at least a subgroup of malignant astrocytic tumours that do not contain amplification of the EGF-receptor. The expression of PDGF alpha-receptors is related to tumour progression in these tumours, and some of the most malignant tumours were shown to contain amplification of the PDGF alpha-receptor. It is also clear now from several experimental studies that PDGF can drive the transformed phenotype, and that PDGF antagonists, by blocking the PDGF autocrine pathway revert the transformed phenotype of certain tumour cells. Because of the findings that receptor protein tyrosine kinases such as the EGF- and the PDGF-receptor play a crucial role in the development of gliomas, it is possible that inhibitors of the phosphorylation of the protein tyrosine kinases will be future candidates for glioma therapy. They might be able to at least delay the development of a fully malignant glioma. The role of PDGF in other tumours of neuroglial origin in the central nervous system has not been studied as extensively as its role in gliomas. Recent data suggest that also for the primitive neuroectodermal tumours overexpression of the PDGF alpha-receptor is related to malignancy of the tumours. For other tumours, such as neuroblastomas, PDGF exerts a differentiating rather than a mitogenic function and is an important survival factor. Further studies are needed to elucidate the role of PDGF in these non-glial primary brain tumours. Moreover, for a complete understanding of the role of PDGF in malignancies of the CNS, it is important to explore its function in the development of the normal CNS further.
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| 8. |
- Smits, A, et al.
(författare)
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Platelet-derived growth factor (PDGF) in primary brain tumours of neuroglial origin.
- 1998
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Ingår i: Histology and histopathology. - 0213-3911. ; 13:2, s. 511-20
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Forskningsöversikt (refereegranskat)abstract
- It has become clear that disruptions in the genome of somatic cells play a causative role in tumour development. We know that the ultimate formation of a malignancy is the result of a multistep process in which the functional loss and/or the altered or increased expression of genes play important roles. One such family of genes are the oncogenes, encoding protein products with mainly growth stimulating effects. Platelet-derived growth factor (PDGF) belongs to the family of oncogenes. It is likely that PDGF plays an essential role in the development of at least a subgroup of malignant astrocytic tumours that do not contain amplification of the EGF-receptor. The expression of PDGF alpha-receptors is related to tumour progression in these tumours, and some of the most malignant tumours were shown to contain amplification of the PDGF alpha-receptor. It is also clear now from several experimental studies that PDGF can drive the transformed phenotype, and that PDGF antagonists, by blocking the PDGF autocrine pathway revert the transformed phenotype of certain tumour cells. Because of the findings that receptor protein tyrosine kinases such as the EGF- and the PDGF-receptor play a crucial role in the development of gliomas, it is possible that inhibitors of the phosphorylation of the protein tyrosine kinases will be future candidates for glioma therapy. They might be able to at least delay the development of a fully malignant glioma. The role of PDGF in other tumours of neuroglial origin in the central nervous system has not been studied as extensively as its role in gliomas. Recent data suggest that also for the primitive neuroectodermal tumours overexpression of the PDGF alpha-receptor is related to malignancy of the tumours. For other tumours, such as neuroblastomas, PDGF exerts a differentiating rather than a mitogenic function and is an important survival factor. Further studies are needed to elucidate the role of PDGF in these non-glial primary brain tumours. Moreover, for a complete understanding of the role of PDGF in malignancies of the CNS, it is important to explore its function in the development of the normal CNS further.
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| 9. |
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| 10. |
- Wollina, U, et al.
(författare)
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Expression of transforming growth factor beta isoforms and their receptors during hair growth phases in mice.
- 1996
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Ingår i: Histology and histopathology. - 0213-3911. ; 11:2, s. 431-6
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor beta (TGF-beta) is a family of potent growth inhibitor proteins, often produced as a precursor and often secreted in a complex with the latent TGF-beta binding protein (LTBP). We investigated the expression of TGF-beta 1, -beta 2, -beta 3, LTBP, TGF-beta receptor proteins type I and type II (T beta R-I and -II) during induced hair growth in C57 BL-6 mice. We here demonstrated that TGF betas and T beta R-I are expressed in hair follicle epithelium and have found a positive reactivity for LTBP and T beta R-I in ++sebocytes. Dermal tissue was weakly stained for LTBP and TGF-beta 3. In early anagen the inner hair root sheath epithelium expressed TGF-beta 1, whereas outer hair root was positive for T beta R-I during anagen/catagen switch. T beta R-II was found in sebaceous glands without significant variations during the hair cycle. We may conclude that in follicle epithelium TGF-beta 1 is not produced in a complex together with LTBP. On the other hand, it is possible that other types of LTBP, like LTBP-2 and LTBP-3, are present, which are not detected by the antibody we used. Furthermore, a very rapid secretion of LTBP from producing cells may prevent immunohistochemical detection. TGF-beta 1 released by inner hair root sheath may regulate outer root sheath growth. A bidirectional interaction of sebocytes and hair follicle epithelium in the TGF-beta/LTBP seems possible. Sebocytes can be considered to be a target for TGFs since they express both T beta R++-I and -II. The general properties of TGF-beta as a growth inhibitor of epithelial cells may suggest a possible involvement in either the abrogation of extensive growth at the end of anagen or the initiation of catagen for the follicle epithelium as well as growth control for sebaceous glands.
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