Preeclampsia is characterized by an exaggerated systemic inflammatory state as well as shallow placentation. In the decidual implantation site , preeclampsia is accompanied by an excessive number of both macrophages and dendritic cells as well as their recruiting chemokines, which have been implicated in the impairment of endovascular trophoblast invasion. Granulocyte-macrophage colony-stimulating factor is known to regulate the differentiation of both macrophages and dendritic cells, prompting both in vivo and in vitro evaluation of granulocyte-macrophage colony-stimulating factor expression in human decidua as well as in a mouse model of preeclampsia. This study revealed increased granulocyte-macrophage colony-stimulating factor expression levels in preeclamptic decidua. Moreover, both tumor necrosis factor-␣ and interleukin-1 ␤, cytokines that are implicated in the genesis of preeclampsia, markedly up-regulated granulocyte-macrophage colony-stimulating factor production in cultured first-trimester human decidual cells. The conditioned media of these cultures promoted the differentiation of both macrophages and dendritic cells from a monocyte precursor. Evaluation of a murine model of preeclampsia revealed that the decidua of affected animals displayed higher levels of immunoreactive granulocyte-macrophage colony-stimulating factor as well as increased numbers of both macrophages and dendritic cells when compared to control animals. Because granulocyte-macrophage colony-stimulating factor is a potent inducer of differentiation and activation of both macrophages and dendritic cells , these findings suggest that this factor plays a crucial role in the pathogenesis of preeclampsia. (Am J

Preeclampsia is associated with increased systemic inflammation and superficial trophoblast invasion, which leads to insufficient utero-placental blood flow. Interleukin (IL)-11 mediates pro- and anti-inflammatory processes and facilitates decidualization. To identify IL-11 expression in vivo at the maternal-placental interface in preeclampsia and control specimens and evaluate regulatory effects of TNF (tumor necrosis factor)-α and IL-1β, cytokines elevated in preeclampsia, on IL-11 levels in first trimester decidual cells in vitro. Placental sections were immunostained for IL-11. Leukocyte-free first trimester decidual cells were incubated with estradiol (E2) ±10−7 mol/L medroxyprogesterone acetate (MPA) ± TNF-α or IL-1β ± inhibitors of the p38MAPK, nuclear factor-kappa B (NFκB), or protein kinase C (PKC) signaling pathways. An ELISA assessed secreted IL-11 levels, and quantitative RT-PCR measured IL-11 mRNA. IL-11 immunoreactivity in placental sections was significantly higher in the cytoplasm of preeclamptic decidual cells versus gestational age-matched controls. Compared to decidual cells, IL-11 immunostaining in neighboring trophoblast is lower, perivascular and not different between control and preeclamptic specimens. TNF-α and IL-1β enhanced levels of IL-11 mRNA and secreted IL-11 in cultured decidual cells. Specific inhibitors of the p38 MAPK and NFκB but not PKC signaling pathways reduced the stimulatory effect of IL-1β. Expression of decidual IL-11 is increased in preeclampsia and suggests a role for IL-11 in the pathogenesis of preeclampsia.

Study DesignA retrospective study.PurposeThe aim of this study was to evalute the effects of mitomycin-C, sodium hyaluronate and human amniotic fluid on preventing spinal epidural fibrosis.Overview of LiteratureThe role of scar tissue in pain formation is not exactly known, but it is reported that scar tissue causes adhesions between anatomic structures. Intensive fibrotic tissue compresses on anatomic structures and increases the sensitivity of the nerve root for recurrent herniation and lateral spinal stenosis via limiting movements of the root. Also, neuronal atrophy and axonal degeneration occur under scar tissue.MethodsThe study design included 4 groups of rats: group 1 was the control group, groups 2, 3, and 4 receieved antifibrotic agents, mitomycin-C (group 2), sodium hyaluronate (group 3), and human amniotic fluid (group 4). Midline incision for all animals were done on L5 for total laminectomy. Four weeks after the surgery, the rats were sacrificed and specimens were stained with hematoxylin-eosin and photos of the slides were taken for quantitive assesment of the scar tissue.ResultsThere was no significant scar tissue in the experimental animals of groups 2, 3, and 4. It was found that there was no significant difference between drug groups, but there was a statistically significant difference between the drug groups and the control group.ConclusionsThis experimental study shows that implantation of mitomycin-C, sodium hyaluronate and human amniotic fluid reduces epidural fibrosis and adhesions after spinal laminectomy in rat models. Further studies in humans are needed to determine the complications of the agents researched.

Amaç: Bu çalışmada, abdominal aort cerrahisinde iskemi/ reperfüzyon (İ/R) sonrası uzak organ hasarı olarak akciğer üzerine silostazol, levosimendan ve bu ilaçların kombinasyonunun etkileri araştırıldı.Ça lış ma pla nı: Çalışma ortalama 219±26 g ağırlığında 35 erkek Wistar albino türü sıçan ile gerçekleştirildi. Sıçanlar her bir grupta yedi sıçan olacak şekilde randomize olarak beş gruba ayrıldı. Sıçanlara silostazol, levosimendan ve bu iki ilacın kombinasyonu ile tedavi uygulandıktan sonra, infrarenal aortik oklüzyon ile alt ekstremitelere 120 dakika iskemi ve sonrasında 60 dakika reperfüzyon uygulandı. Sıçanlar derin anestezi altında sakrifiye edildi ve akciğer dokuları çıkarıldı. Akciğer dokularında malondialdehid (MDA) düzeyleri, süperoksit dismutaz (SOD) aktiviteleri ve glutatyon (GSH) düzeyleri ölçüldü. Doku örnekleri ayrıca ışık mikroskobu ile histopatolojik olarak incelendi. Bul gu lar:Çalışmada İ/R'nin akciğer dokusunda MDA düzeylerini yükseltirken, SOD aktivitesini ve GSH düzeylerini azalttığı belirlendi (p<0.05). Silostazol, levosimendan ve bu ilaçların kombinasyonu ile MDA düzeyleri, SOD aktiviteleri, GSH düzeyleri ve akciğer hasarı skorunda iyileşme gözlendi (p<0.05). Bu ilaçların tek veya kombine kullanılması arasında anlamlı farklılık yoktu (p>0.05). So nuç:Bu bulgular ışığında, vasküler cerrahi sırasında ekstremite iskemisi öncesi silostazol ve levosimendan kullanımı akciğer dokusunu İ/R hasarından korumakta faydalı olabilir. Bununla birlikte, bu iki ilacın kombine kullanımı, İ/R hasarına karşı koruyuculuğu artırmamaktadır.Anah tar söz cük ler: Abdominal aort; silostazol; iskemi-reperfüzyon; levosimendan; akciğer hasarı.Background:In this study, we aimed to investigate the effects of cilostazol and levosimendan, and the combination of these agents on the lung remote organ damage after ischemia/reperfusion (I/R) following abdominal aortic surgery. Methods:The experiments were performed on 35 male Wistar albino rats weighing mean 219±26 g. The rats were randomly assigned into five groups, including each of seven rats. Rats were pretreated with cilostazol and levosimendan, alone or in combination, and then lower extremities were subjected to I/R induced by a infrarenal aortic occlusion for duration of 120 minutes, followed by a-60 minute-reperfusion. The rats were sacrificed under deep anesthesia and the lung tissues were removed. Malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and glutathione (GSH) levels were measured in the lung tissues. The tissue samples were further examined histopathologically under light microscopy.Results: It was found that I/R elevated MDA levels accompanied by a reduction in SOD activities and GSH levels (p<0.05). Cilostazol and levosimendan, and their combination restored MDA levels, SOD activity, GSH levels and lung injury scores (p<0.05). There was no significant difference among individual or combined treatment of these agents (p>0.05). Conclusion:In light of these findings, cilostazol and levosimendan may be useful for protecting the lung tissue from...