The processes of digestion in the avian gastrointestinal tract depend on sophisticated control systems that co-ordinate secretion of digestive juices and movement of the luminal contents. In the current study, the distribution of serotonin-, gastrin-, glucagon-and somatostatin-immunoreactive endocrine cells was investigated by immunocytochemical methods in the intestinal tract of the goose. The number of cells immunoreactive for each antiserum was evaluated in different regions of the intestinal tract. Serotonin-, glucagon-and somatostatinimmunoreactive endocrine cells were seen throughout the intestinal tract, but somatostatin-immunoreactive cells were not detected in the colon of the goose. Gastrin-immunoreactive cells were detected only in the duodenum, jejunum and colon mucosa. It is concluded that the distribution pattern of the entero-endocrine cells in the goose is similar to that of most of the mammalian and other poultry species.
The objective of the present study was to determine the effects of follistatin addition on myostatin and follistatin gene expression patterns in C 2 C 12 muscle cells. C 2 C 12 cells were administered with 100 ng/ml recombinant human (rh) follistatin in Dulbecco's modified Eagle medium (DMEM) containing 10% fetal bovine serum (FBS), 4 mM glutamine and antibiotics daily for three days. Rh follistatin was not added in the control wells. Follistatin and myostatin gene cDNAs were synthesised by reverse transcriptase polymerase chain reaction (RT-PCR). The time course of follistatin gene expression pattern was similar in both the control and the follistatin-treated group. Myostatin mRNA level significantly increased in the follistatin-treated group after 24 h of culture ( Fig. 3, P < 0.01). Amounts then sharply decreased (Fig. 3, P < 0.01) at 48 h of culture, whereas there was no significant difference between the control and the follistatin-treated group at 72 h of culture. Our results demonstrated that myostatin and follistatin mRNA were expressed in C 2 C 12 cells and rh follistatin changed the myostatin expression pattern.
Although preeclampsia (PE) is one of the most important problems affecting pregnant women, etiologic factors in its development are still unclear. We aimed to investigate the expression levels of platelet endothelial cell adhesion molecule-1 (PECAM-1) and intercellular adhesion molecule-1 (ICAM-1) in preeclamptic and control healthy placentas. Placental tissue samples were obtained after delivery from patients diagnosed with PE, and from normal term pregnants and analyzed by immunohistochemistry for the expression levels of the two adhesion molecules PECAM-1 and ICAM-1. A strong expression of PECAM-1 in endothelial cells lining the vessel walls of placental villi in placentas of control group was found, but the intensity of PECAM-1 expression was highly reduced in placentas of PE group (p = 0.017). Conversely, a strong expression of ICAM-1 was observed in placental villi in PE, significantly higher than that of normal placentas (p = 0.005). The findings of a decrease of PECAM-1 expression and an increase of ICAM-1 expression in preeclamptic placenta suggest the existence of functional roles of these adhesion molecules in the pathophysiology of PE, probably by contributing to the reduced trophoblast invasion and the increased vascular damage, respectively. Inhibiting ICAM-1 (i.e., with ICAM-1 monoclonal antibody) and promoting PECAM-1 expression may be good therapeutic approaches to prevent PE symptoms in the future.
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