Effect of low-level laser therapy (LLLT) on orthodontic tooth movement.

The aim of this study is to evaluate the effects of low-level laser therapy (LLLT) on (1) the velocity of orthodontic tooth movement and (2) the nitric oxide levels in gingival crevicular fluid (GCF) during orthodontic treatment. The sample consisted of 20 patients (14 girls, six boys) whose maxillary first premolars were extracted and canines distalized. A gallium-aluminum-arsenide (Ga-Al-As) diode laser was applied on the day 0, and the 3rd, 7th, 14th, 21st, and 28th days when the retraction of the maxillary lateral incisors was initiated. The right maxillary lateral incisors composed the study group (the laser group), whereas the left maxillary lateral incisors served as the control. The teeth in the laser group received a total of ten doses of laser application: five doses from the buccal and five doses from the palatal side (two cervical, one middle, two apical) with an output power of 20 mW and a dose of 0.71 J /cm(2). Gingival crevicular fluid samples were obtained on the above-mentioned days, and the nitric oxide levels were analyzed. Bonferroni and repeated measures variant analysis tests were used for statistical analysis with the significance level set at p ≤ 0.05. The application of low-level laser therapy accelerated orthodontic tooth movement significantly; there were no statistically significant changes in the nitric oxide levels of the gingival crevicular fluid during orthodontic treatment.

The therapeutic effects of melatonin and nimodipine in rats after cerebral cortical injury.

AIM: Secondary brain injury starts after the initial traumatic impact and marked by an increase in the intracellular calcium concentrations.This cascadeeventually results in membrane lipid peroxidation and neuronal cell death. MATERIAL AND METHODS: We investigated the neuro-protective effects of nimodipine and melatonin in 38 rats after 6 hours of head trauma using the cortical impact injury model of Marmarou. RESULTS: Brain water in the melatonin-given group decreased significantly comparing to that of control group the brain water in the nimodipine given group increased significantly comparing to that of trauma group. Histopathologically, brain edema was significantly low in melatonin-administered group comparing to that of control group while there were no changes in brain edema in the nimodipine given group and in the group that both nimodipine and melatonin were administered in combination. MDA levels in the brain tissues were significantly lower in the melatonin and nimodipine groups comparing to those of trauma and control group however this difference was by far significant in melatonin group comparing to nimodipine group. CONCLUSION: Melatonin appears to have neuro-protective effects on the secondary brain damage while nimodipine and nimodipine plus melatonin combination did not show such neuro-protective effects on the secondary brain injury.

Therapeutic efficacy of intraventricular cyclosporine A and methylprednisolone on a global cerebral ischemia model in rats.

OBJECTIVE: Cyclosporine A (CsA) with its immunosuppressive actions and methylprednisolone (MP) as a free radical scavenger were suggested together to alleviate neural tissue damage after an ischemic insult. The aim of this study was to investigate neuroprotective properties of CsA and MP in a global cerebral ischemia model. METHODS: Twenty-eight male Sprague-Dawley rats were divided randomly into four separate groups: CsA, MP, sham and control. Global cerebral ischemia was performed with the four-vessel occlusion model. After 30 minutes of ischemia, reperfusion was started with concomitant intraventricular administration of saline, MP (20 mg/kg) and CsA (10 mg/kg) into the lateral ventricle. Lipid peroxidation levels were measured from all experimental groups. Rats subjected to global cerebral ischemia exhibited a significant increase in cerebral lipid peroxide levels 6 hours after the onset of reperfusion. Both CsA and MP treatment significantly attenuated the degree of lipid peroxidation in cerebral tissues (p<0.05). Histopathological examinations of the CA1 sector of the hippocampus verified the neuroprotective properties of MP and CsA. CONCLUSIONS: The results suggested the neuroprotective properties of both agents, emphasizing more potent protection against ischemia by CsA. It was proposed that CsA could have exerted this effect with the blockage of mitochondrial permeability transition (MPT) pores, which are also critical if the necrotic and apoptotic cascades of the cell are considered. MP is judged to be neuroprotective, particularly in terms of its effects on lipid peroxidation. In conclusion, CsA and MP are ascertained to be neuroprotective agents as long as they cross the blood-brain barrier.

Selenium treatment protects diabetes-induced biochemical and ultrastructural alterations in liver tissue.

We have shown that a single dose of streptozotocin (STZ) (50 mg/kg body weight) injected into rats caused significant changes in some antioxidant enzyme activities, such as glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase activities, and acid-soluble sulfhydryl levels of the liver tissue with respect to the control rats. Furthermore, these alterations in the activities of the antioxidant enzymes were accompanied by significant changes in the ultrastructure of the liver tissue; mainly intercellular biliary canaliculi were distended and contained stagnant bile, swollen mitochondria in hepatocytes and disoriented and disintegrating cristae, dilatation of the rough endoplasmic reticulum (rER) with detachment of ribosomes, and dissociation of polysomes. Both diabetic and normal rats were treated with sodium selenite (5 micromol/kg/d, intra peritoneally) for 4 wk following 1 wk of diabetes induction. This treatment of diabetic rats improved significantly diabetes-induced alterations in liver antioxidant enzymes. Moreover, treating of diabetic rats with sodium selenite prevented primarily the variation in staining quality of hepatocytes nuclei, increased density and eosinophilia of the cytoplasm, focal sinusoidal dilatation and congestion, and increased numbers of mitochondria with different size and shape. In summary, treatment of diabetic rats with sodium selenite has beneficial effects on both antioxidant system and the ultrastructure of the liver tissue. These findings suggest that diabetes-induced oxidative stress can be responsible for the development of diabetic complications and antioxidant treatment can protect the target organs against diabetes.