Evaluation of the Association Between Matrix Metalloproteinase 11 and Intervertebral Disc Disease.

AIM: The intervertebral disc starts to degenerate when a human being begins to stand and learn to walk. It is known that many extrinsic, intrinsic and genetic factors play a role in disc degeneration. In this study, we examined whether the matrix metalloproteinase 11 might be associated with intervertebral disc degeneration. MATERIAL AND METHODS: Fifty-six patients with lumbar disc herniations who were operated at Göztepe Education and Research Hospital, Neurosurgery Clinic between September 2008 and December 2009 were prospectively reviewed. History and complaints were obtained from the case reports. Neuroradiological evaluation was performed with magnetic resonance imaging. Surgical findings of cases were reported in the operation notes. Microscopic posterior hemipartial laminectomy and discectomy were performed in all cases. Degenerated herniated disc material of all cases extracted during surgery was evaluated with immunohistochemical staining in Marmara University, Institute of Neurological Sciences, Pathology Laboratory. RESULTS: Comparing the immunohistochemical staining of cases who were 50 years or younger and cases who were over 50 years old, statistical significance was determined. CONCLUSION: Matrix metalloproteinase 11 has a role in degenerating intervertebral disc disease, but it is not the only factor. Matrix metalloproteinase 11 might be a genetic factor in young-middle aged patients.

High angiogenic potential in an in vivo rat corneal model is associated with shorter disease-free survival in low-grade oligodendrogliomas.

This study aimed to examine the association between time to tumor recurrence, angiogenic potential and tumor contrast-enhancement. Tumor samples were taken from 20 patients with low-grade oligodendroglioma and examined for their angiogenic potential using an in vivo rat corneal model of angiogenesis. Patients were evaluated for tumor contrast enhancement prior to surgical excision using MRI and they were followed for tumor recurrence. Patients who had tumors without contrast enhancement had longer disease-free survival (median time to tumor recurrence, 72 months) compared to those who had tumors with contrast enhancement (median, 42 months; p=0.0068). Based on corneal angiogenesis assay results, a high angiogenic potential was associated with a significantly shorter disease-free survival. Our findings suggest that radiological contrast enhancement and a high angiogenic potential based on an in vivo corneal angiogenesis assay were related to a shorter disease-free survival. This might have important prognostic implications in patients with low-grade oligodendrogliomas.

Whey feeding suppresses the measurement of oxidative stress in experimental burn injury.

PURPOSE: Burns cause thermal injury to local tissue and trigger systemic acute inflammatory processes, which may lead to multiple distant organ dysfunction. We investigated the protective effect of dietary whey supplementation on distant organs in a rat model. METHODS: Forty-eight rats were divided into six groups of eight: groups 1 and 2 were the controls, fed a standard diet and a whey-supplemented diet, respectively; groups 3 and 4 were fed a standard diet and subjected to burn injury; and groups 5 and 6 were fed a whey-supplemented diet and subjected to burn injury. We measured the oxidative stress variables, as well as glutathione in the liver and kidney, and histologically examined skin samples obtained 4 h (groups 3 and 5) and 72 h (groups 4 and 6) after burn injury. RESULTS: Glutathione (GSH) levels remained the same in the liver but were slightly elevated in the kidneys after burn injury in the rats fed a standard diet. Whey supplementation caused a significant increase in hepatic GSH levels 4 h after burn injury. Moreover, there was a significant rebound effect in the liver and kidney GSH levels after 72 h and whey supplementation potentiated this effect. Hepatic and renal lipid peroxide levels were also increased 4 h after burn injury in the rats fed a standard diet. Whey supplementation significantly suppressed the burn-induced increase in hepatic and renal lipid peroxide levels. Histological examination revealed that although whey supplementation resulted in decreased subepidermal inflammation, the indicators of wound healing and collagen deposition were not improved. CONCLUSION: Whey pretreatment suppressed hepatic and renal oxidative stress measurements after experimental burn injury.

Collagen ultrastructure and TGF-beta1 expression preserved with aminoguanidine during wound healing in diabetic rats.

Advanced glycoxidation end products have been implicated in delayed diabetic wound healing. In this study, we evaluated the effects of aminoguanidine, which is an advanced glycation and nitric oxide (NO) synthase inhibitor, on extracellular matrix protein expression, collagen configuration, and nitrite/nitrate levels in wounds of diabetic rats. Sixteen Wistar male rats were made diabetic by streptozotocin. Of these, eight rats were given AG (aminoguanidine bicarbonate (AG) (group DAG) in their drinking water, and eight rats were followed as diabetic paired controls (group D). Eight healthy rats were followed as the healthy control group (group H). At the eighth week, a 2 x 2 cm area full-thickness skin defect was created. The degree of contraction of the open wounds was evaluated for 2 weeks duration. On the 15th postoperative day, wound surface areas were measured, and wound specimens and blood samples were collected. The shrinking percentage of the wounds was small in both groups H and DAG compared with group D (p < 0.05). Similar to healthy rats, the aminoguanidine-treated diabetic rats had very strong transforming growth factor (TGF)-beta1 expression in granulation tissue and intact skin in comparison with diabetic controls. In the diabetic group, the intact skin demonstrated sparsely distributed regular collagen fibers in the granulation zone, and the regular pattern of collagen fibers was lost. In conclusion, aminoguanidine improves wound healing, restores growth factor TGF-beta1 expression, and preserves collagen ultra structure, whereas it has no prominent effect on NO levels within wound tissue in diabetic rats.