Expression of intercellular adhesion molecule-1 in umbilical and placental vascular tissue of gestational diabetic and normal pregnancies.

OBJECTIVE: Expression of intercellular adhesion molecule-1 (ICAM-1), a marker of endothelial dysfunction leading to damaging vascular disorders, in umbilical and placental vascular tissue of gestational pregnancies was compared to non-diabetic controls. METHODS: We included 32 pregnant women with gestational diabetes mellitus (GDM) and 28 women with normal ongoing pregnancies were taken as the control group. Pregnant women with GDM were selected from the ones who had glycosylated haemoglobin (HbA(1c)) values lower from 6%. CD54/ICAM-1 expression profile was evaluated by immunohistochemistry, and cellular localization was determined under light microscopy. The immunoreactivity was assessed using a four-tiered scale: 0-5% (0), 6-20% (+1), 21-50% (+2), 51-100% (+3). RESULTS: In gestational diabetic patient's umbilical artery, +1 immunostaining group was observed (62.5%), and in their placenta, the highest percentage was seen in the 0 immunostaining group (43.8%). Diabetic patient's umbilical vein has the highest percentage in the +1 immunostaining group. In the control group, in both umbilical artery and vein, the highest percentage was seen in the +2 immunostaining group (46.4%) and their placenta has the +3 immunostaining group with the highest percentage (57.1%). CONCLUSION: The main outcome of our study was that, although underlying diabetes does have some effects on the pregnant mother, fears of endothelial dysfunction leading to damaging vascular disorders are probably unfounded in well-controlled GDM women.

The role of fibroblast growth factor-2 in healing the dura mater after inducing cerebrospinal fluid leakage in rats.

We conducted a study to determine the effectiveness of topically applied recombinant mouse fibroblast growth factor-2 (FGF-2) in healing the dura mater in a rat with dura mater injury and cerebrospinal fluid leakage. Laminectomies were performed in 32 rats at the level of the L2-L4 vertebrae, and a dura mater defect was created. Sixteen rats were treated postoperatively with locally applied recombinant mouse FGF-2, and 16 animals received normal saline. FGF-2 effects on dura mater healing, cerebrospinal fluid leakage, and wound healing were assessed at 3 and 6 weeks postoperatively. The extent of dura mater healing was evaluated by histological analysis. We found that dura mater healing was significantly increased (p<0.05) in rats treated with FGF-2 compared with rats in the control group. In this experimental model, locally applied FGF-2 effectively increased dura mater healing and induced no side effects.

The effects of topical granulocyte-macrophage colony-stimulating factor on dural healing in rats after induced cerebrospinal fluid leakage.

OBJECT: Dural defects must be repaired to protect the central nervous system from contamination. Although there are various experimental and commercial substances available for this purpose, the ultimate method of watertight dural closure has yet to be discovered. In this study, the authors investigate the effects of topically applied recombinant mouse granulocyte-macrophage colony-stimulating factor (GM-CSF) on dural healing in a rat model of dural injury and cerebrospinal fluid leakage. METHODS: In this experimental model, a dural defect at the level of the L1-2 vertebrae was created in 32 Wistar rats. Sixteen animals were treated with locally applied recombinant mouse GM-CSF postoperatively, and 16 animals received normal saline. The effects of GM-CSF on dural healing, cerebrospinal fluid leakage, and wound healing were assessed 2 and 4 weeks postoperatively. Dural healing was evaluated histologically. RESULTS: Dural healing was increased in rats treated with GM-CSF compared with rats in the control group. This difference was statistically significant (p < 0.05). CONCLUSIONS: Cerebrospinal fluid leakage may impede healing of dural defects. Topically applied GM-CSF seems to aid in dural healing.

Neuroprotective effects of infliximab in experimental spinal cord ischemic injury.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia-reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin-eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups (p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups (p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant (p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.