The Distribution of Foxp3 and CD68 in Preeclamptic and Healthy Placentas: A Histomorphological Evaluation.

Preeclampsia is a complication of pregnancy that affects 3-5% of pregnancies and is one of the major causes of maternal/neonatal mortality and morbidities worldwide. We aimed to investigate the distribution of Foxp3+ regulatory T-cells and CD68+ Hofbauer cells in the placenta of preeclamptic and healthy pregnant women with a special focus on correlating these findings with placental histology. Decidua and chorionic villi of the placenta obtained from healthy and preeclamptic pregnancies were evaluated in full-thickness sections. Sections were stained with hematoxylin and eosin and Masson's trichrome and immunostained for Foxp3 and CD68 for histological analyses. The total histomorphological score for placentas was found to be higher in preeclamptic placentas than that in the controls. The CD68 immunoreactivity was higher in the chorionic villi of preeclamptic placentas than that in the controls. The immunoreactivity of Foxp3 was found widely distributed within the decidua in both the groups and did not differ significantly. Interestingly, Foxp3 immunoreactivity in the chorionic villi was found mainly in the villous core and, to a lesser extent, in the syncytiotrophoblasts. We found no significant relation between Foxp3 expressions and morphological changes observed in preeclamptic placentas. Although extensive research is being carried out regarding the pathophysiology of preeclampsia, the findings are still controversial.

The Effect of Alpha Lipoic Acid on the Recovery of Sciatic Nerve Injury in Rats: A Prospective Randomized Controlled Trial.

OBJECTIVE: The aim of this study was to investigate the regenerative effects of alpha lipoic acid on the recovery of sciatic nerve crush injury (SNCI) in rats. DESIGN: This was a randomized, experimental, and sham-controlled study. The sciatic nerves of 28 rats in four groups were traumatized for 60 secs: G1, sham operated + saline; G2, SNCI + saline; G3, SNCI + alpha lipoic acid 50 mg/kg/day; and G4, SNCI + alpha lipoic acid 100 mg/kg/day. Sciatic functional index values were measured on day 0, 1, 7, 14, 21, and 28. Sciatic nerve stimulation threshold values were recorded on day 1, 14, and 28. End-point histopathologic evaluation was conducted. RESULTS: The mean sciatic functional index value of G2 but not G3/G4 on day 7 was significantly lower than on day 0 (P = 0.035, P = 0.447/P = 0.800). The mean sciatic functional index value of G2 but not G3/G4 increased significantly between day 7 and 14 (P = 0.035, P = 0.447/P = 0.438). The day 14 mean sciatic nerve stimulation threshold values of G3/G4 but not G2 were decreased significantly compared with those on day 1 (P = 0.022/P = 0.022, P = 0.933). The mean sciatic nerve stimulation threshold values of G3/G4 on day 14 were similar to those on day 0 (P = 0.106/P = 0.418). Regeneration in muscle and nerve connective tissues and nerve structures was observed in G3/G4. Inflammation in the muscle and nerve tissues of G4 was suppressed down to similar levels of G1. Myelinated nerve fibers were less degenerated in G3/G4. CONCLUSION: Alpha lipoic acid has the potential to accelerate the process of nerve healing in the context of SNCI in rats.

Alterations of IL-1 and VEGF After Ischemia-Reperfusion Injured Uterus and Ovary in Rats.

OBJECTIVE: Ischemia/reperfusion injury causes parenchymal and endothelial cell damage as a result of inflammation. Vascular endothelial growth factor (VEGF) expressed in every kind of tissue in human body has important roles in migration, proliferation, endothelial cell permeability, angiogenesis and vasculogenesis. IL-1 is a one of the cytokine family members, and plays important roles in hematopoiesis, inflammatory reactions and immune system regulation. Furthermore, auto-inflammatory diseases are treated by IL-1 as therapeutic agent. The aim of this study is to observe changes of VEGF and IL-1 immunreactivity in ischemia/reperfused rat uterus and ovary. METHOD: Rats were separated into two groups. Control group and ischemia/reperfusion group which rats were subjected to 45 min ischemia/45 min reperfusion. Samples from uterus and ovary were fixed with 10% neutral formaldehyde and stained with H&E. VEGF and IL-1 immunohistochemistry was applied. RESULTS: Histopathological results showed severe degeneration of endometrium in uterus and ovarian follicles in ischemia/reperfusion group. VEGF and IL-1 immunoreactivity increased in uteruses and ovaries of ischemia/reperfusion group when compared to control group. CONCLUSION: In consequence, the present results suggest that VEGF and IL-1 may be potential detection marker for ischemia/reperfusion injured uterus and ovary. Moreover, VEGF and IL-1 might be in relation with each other to regenerate uterus and ovary.

Distribution of Zonula Occludens-1 and Occludin and alterations of testicular morphology after in utero radiation and postnatal hyperthermia in rats.

In utero irradiation (IR) and postnatal hyperthermia (HT) exposure cause infertility by decreasing spermatogenic colony growth and the number of sperm in rats. Four groups were used: (i) Control group, (ii) HT group (rats exposed to hyperthermia on the 10th postnatal day), (iii) IR group (rats exposed to IR on the 17th gestational day) and (iv) IR + HT group. Three and six months after the procedures testes were examined by light and electron microscopy. Some degenerated tubules in the HT group, many vacuoles in spermatogenic cells and degenerated tight junctions in the IR group, atrophic tubules and severe degeneration of tight junctions in the IR + HT group were observed. ZO-1 and occludin immunoreactivity were decreased and disorganized in the HT and IR groups and absent in the IR + HT group. The increase in the number of apoptotic cells was accompanied by a time-dependent decrease in haploid, diploid and tetraploid cells in all groups. Degenerative findings were severe after 6 months in all groups. The double-hit model may represent a Sertoli cell only model of infertility due to a decrease in spermatogenic cell and alterated blood-testis barrier proteins in rat.