Effect of Topical Platelet-Rich Plasma on Burn Healing After Partial-Thickness Burn Injury.

BACKGROUND To investigate the effects of platelet-rich plasma on tissue maturation and burn healing in an experimental partial-thickness burn injury model. MATERIAL AND METHODS Thirty Wistar albino rats were divided into 3 groups of 10 rats each. Group 1 (platelet-rich plasma group) was exposed to burn injury and topical platelet-rich plasma was applied. Group 2 (control group) was exposed to burn injury only. Group 3 (blood donor group) was used as blood donors for platelet-rich plasma. The rats were killed on the seventh day after burn injury. Tissue hydroxyproline levels were measured and histopathologic changes were examined. RESULTS Hydroxyproline levels were significantly higher in the platelet-rich plasma group than in the control group (P=.03). Histopathologically, there was significantly less inflammatory cell infiltration (P=.005) and there were no statistically significant differences between groups in fibroblast development, collagen production, vessel proliferations, or epithelization. CONCLUSIONS Platelet-rich plasma seems to partially improve burn healing in this experimental burn injury model. As an initial conclusion, it appears that platelet-rich plasma can be used in humans, although further studies should be performed with this type of treatment.

The protective effect of L-carnitine on hepatic ischemia-reperfusion injury in rats.

BACKGROUND/AIMS: Ischemia-reperfusion injury may occur during liver transplantation and remains a serious concern in clinical practice. This study was designed to study the potential benefit of L-carnitine on experimental warm hepatic ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Forty-five male Wistar Albino rats were divided into three groups; Group 1 sham-operation without ischemia-reperfusion (n=15); Group 2, ischemia-reperfusion (n=15); and Group 3, which was administered L-carnitine (200 mg/kg, intraperitoneal, for 4 days) prior to ischemia-reperfusion (n=15). The study animals were then sacrificed to obtain hepatic tissue and serum samples. Tissue levels of malondialdehyde and reduced glutathione and serum levels for aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were assessed. RESULTS: Mean aspartate aminotransferase levels were significantly higher in Group 2 (405.2 U/L) when compared to Groups 1 (137.1 U/L) and 3 (267.6 U/L). Mean alanine aminotransferase levels were significantly higher in Group 2 (257.1 U/L) when compared to Groups 1 (37.2 U/L), and 3 (118.1 U/L) (p< 0.001 for each). Mean lactate dehydrogenase levels were significantly higher in Group 2 (2943.8 U/L) when compared to Groups 1 (1496.5 U/L), and 3 (2185.3U/L) (p < 0.001 for each). Mean malondialdehyde levels were significantly higher in Group 2 (54.3 nmol/g) compared to Groups 1 (41.0 nmol/g) and 3 (42.1 nmol/g) (p < 0.001 for each). Mean reduced glutathione levels were significantly lower in Group 2 (5.9 nmol/mg) and Group 3 (7.4 nmol/mg) compared to Group 1 (9.1 nmol/mg) (p < 0.001 for each). CONCLUSIONS: In conclusion, our data supports a protective effect of L-carnitine against oxidative damage in hepatic ischemia-reperfusion injury in rats. This is evidenced by improvement of the antioxidant defense system and lipid peroxidation levels.

Wound healing at adaptation zones of skin flaps harvested from acute burned skin.

BACKGROUND: Early reconstruction of burn defects culminates in more successful results. The wound healing process of the burned skin affects not only the curative phase of the burned area but also result of any reconstructive procedure including the regional flaps. Thus, in this study, we have evaluated the wound healing process at the distal incisions of random-pattern skin flaps prepared from burned dorsal skin of rats. MATERIALS AND METHODS: Thermal burn damage was performed with dimensions of 3cm×3cm on Wistar albino rats. In group 1 (n=12), no burn was produced and 3cm×3cm caudally based, random-pattern skin flaps were elevated. In group 2 (n=12), a 5cm×5cm area of partial-thickness thermal damage was produced and after three days a 3cm×3cm random-pattern skin flap was elevated as in group 1 inside the burned skin site. In group 3 (n=12), 3cm×3cm area of partial-thickness thermal damage was produced and after three days 3cm×3cm random-pattern skin flap was elevated. In group 4 (n=12), 3cm×3cm area of partial-thickness thermal damage was produced and after three days a 3cm×3cm random-pattern skin flap was elevated at the distal margin of the burned area. The flaps were adapted to the donor sites in all groups. The histopathological evaluation was done and hydroxyproline levels were measured. RESULTS: There were no significant differences between groups regarding presence of epithelialization, myofibroblast numbers, and collagen texture (p>0.05). Neovascularization level was significantly higher in group 2 than the other groups (p<0.05). There were no statistically significant difference among the hydroxyproline levels in all four groups (p>0.05). CONCLUSION: The preference of the incision site in a burn zone while designing a flap during the acute burn period was proposed to possess no difference in terms of wound healing in an animal model.

Minocycline treatment inhibits lipid peroxidation, preserves spinal cord ultrastructure, and improves functional outcome after traumatic spinal cord injury in the rat.

STUDY DESIGN: A prospective, randomized experimental research. OBJECTIVE: To evaluate the short- and long-term neuroprotective effects of minocycline on the secondary injury process of an experimental traumatic spinal cord injury (SCI) model. SUMMARY OF BACKGROUND DATA: Traumatic SCI is a devastating problem of health that results in high morbidity and mortality rates. The loss of function after SCI results from both the primary mechanical insult and the subsequent, multifaceted secondary response. METHODS: A total of 80 adult male Spraque-Dawley rats (breeded by the Baskent University Animal Research Center) were randomly divided into 4 groups. A T10 contusion injury was produced by using modified Allen technique in all groups except the control group. No medication was administered to the rats in the trauma group. Minocycline was administered intraperitoneally and intravenously to the treatment groups. Short-term and/or long-term neuroprotective effects of minocycline on the lipid peroxidation (malondialdehyde, glutathione), apoptosis (terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling), ultrastructure of spinal cord (tissue electron microscopy), and behavioral assessments (Basso-Beattie-Bresnahan) were evaluated. RESULTS: As compared with the trauma group, tissue malondialdehyde and glutathione levels demonstrated that minocycline significantly diminishes lipid peroxidation. Electromicroscopic study showed that minocycline preserves the ultrastructure of spinal cord tissue in the early post-traumatic period. Minocycline treatment significantly reduced the number of terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling positive cells both 1 day and 28 days after SCI. Behavioral assessments showed significant improvement in the hind limb functions of minocycline receiving rats starting 7 days after the SCI. Any statistically significant difference was not found between intraperitoneal or intravenous routes for minocycline injection. CONCLUSION: Minocycline is neuroprotective and contributes to functional improvement after traumatic SCI by eliminating the destructive process of secondary injury. Having both satisfying anti-inflammatory and antiapoptotic effects in experimental models, it promises to be of therapeutic use in human SCI.

Can first-trimester screening program detect women at high risk for gestational diabetes mellitus?

This study was designed to compare first-trimester maternal serum biochemical markers of aneuploidy and fetal nuchal translucency in pregnancies complicated by gestational diabetes mellitus and those of a control group. The study included 60 gestational diabetic and 60 control women who attended the first-trimester combined screening program for Down syndrome between 11 and 14 gestational weeks with complete follow-up data and delivered in our institution. Maternal serum free ß-human chorionic gonadotropin, pregnancy-associated plasma protein-A and fetal nuchal translucency were investigated. The combined risks, double test risks and age risks were calculated by PRISCA software version 4.0. Comparison of the results between the two groups yielded no significant differences in serum levels of free ß-human chorionic gonadotropin and fetal nuchal translucency. However, women who developed gestational diabetes mellitus had significantly lower pregnancy-associated plasma protein-A. And also, the combined risks and double test risks calculated by PRISCA software were statistically higher in gestational diabetic women than normal pregnant women. These results suggest that differences can be seen between diabetic and healthy pregnant women in first-trimester maternal serum biochemical markers of aneuploidy.

Protective role of simvastatin on lung damage caused by burn and cotton smoke inhalation in rats.

BACKGROUND: Smoke inhalation injury is a major comorbid factor in patients with thermal injury and occurs in about 30% of patients with major burns. In addition, inhalation injury reportedly accounts for 20%-84% of the mortality in burned individuals and is associated with higher mortality rates for every age and burn size category. The aim of the present study was to investigate the effects of simvastatin on lung damage with burn and cotton smoke inhalation. METHODS: Wistar rats were randomly assigned to three groups: saline treated control group, via an orogastric route (group 1, n = 6), burn (30%) and cotton smoke inhalated group (group 2, n = 6), and simvastatin treated (25 mg/kg/d, via an orogastric route) burn (30%) and cotton smoke inhalated group (group 3, n = 6). Rats were sacrificed at 48 h of the treatments and the trachea and lungs were removed completely. Tissue samples were taken for histopathologic, immunohistopathologic, and biochemical analyses. Univariate analysis of variance coupled with Duncan's post-hoc test was performed for statistical evaluation. RESULTS: Lung parenchymal and tracheoepithelial damage was confirmed in group 2 by histopathologic examination. Lung malonedialdehyde (MDA) levels were significantly decreased (P < 0.001), while glutathione (GSH) concentration did not alter in group 2 compared with group 1. Also, immunopathologic data revealed that epithelial iNOS level was elevated, while no modulation was detected in the level of myeloperoxidase (MPO). Simvastatin administration resulted in decreasing the lung parenchymal and tracheoepithelial damage. Tissue MDA levels were decreased significantly (P < 0.001), whereas GSH concentrations were elevated in group 3 compared with group 1 and group 2 (P < 0.001). Simvastatin treatment caused a decrease in epithelial iNOS levels, while MPO levels were not modulated. In addition, simvastatin significantly reduced pulmonary apoptosis in lung injury. CONCLUSIONS: Our results have indicated that simvastatin administration seems to play beneficial role in lung injury of rats promoted by combined burn and smoke inhalation. Thus, simvastatin may represent a potential approach to prevent smoke inhalation-associated lung dysfunction. However, the significant decrease in basal oxidant production may cause impairment in cellular signalling processes.

Recombinant human-activated protein C inhibits cardiomyocyte apoptosis in a rat model of myocardial ischemia-reperfusion.

OBJECTIVES: Myocardial apoptosis is recognized as a major mechanism of cell death during ischemia-reperfusion. In this study, we assessed the hypothesis that activated protein C may have a cardioprotective effect via preventing apoptosis in a rat model of myocardial ischemia-reperfusion. METHODS: Thirty male Sprague-Dawley rats were anesthetized, instrumented for hemodynamic measurements and ventilated mechanically. Twenty rats were subjected to 20 min of left anterior descending coronary artery occlusion and 2 h of reperfusion. They were randomly assigned to receive intravenous Ringer lactate (vehicle) or activated protein C (2 mg/kg/h) 10 min after occlusion and during reperfusion. The other 10 rats were sham-operated. At the end of the reperfusion period, serum samples were obtained for evaluation of creatine kinase, C-reactive protein and tumor necrosis factor-alpha. Apoptosis was measured quantitatively by the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling method. RESULTS: Serum creatine kinase, C-reactive protein and tumor necrosis factor-alpha values and percentage of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling- positive myocyte nuclei demonstrated negligible myocardial injury in sham-operated controls. During reperfusion, mean arterial pressures were significantly higher in activated protein C-treated rats than in the control group (68.2+/-10.3 vs. 55.4+/-11.6 mmHg, P=0.01). Number of apoptotic cells was significantly reduced from 47.7 to 24.8% with activated protein C administration (P=0.008). No difference was seen between activated protein C-treated and untreated animals with respect to creatine kinase, C-reactive protein and tumor necrosis factor-alpha levels. CONCLUSIONS: Treatment with activated protein C significantly improved hemodynamics after ischemia-reperfusion and reduced ischemia-reperfusion-induced myocardial apoptosis in rats.

The effect of melatonin treatment on oxidative and nitrosative stress in rats with thioacetamide-induced hepatic damage.

BACKGROUND: : The following study aimed to clarify the importance of arginase and NOS activities in thioacetamide-induced hepatic damage and to evaluate the underlying mechanism of proposed protection provided by melatonin, using commonly applied therapeutic dose. METHODS: : Rats were randomly assigned to four groups (n=5): control, melatonin (10mg/kg i.p.), thioacetamide (200mg/kg i.p., two doses with a 24h interval) and thioacetamide+three doses of melatonin (10mg/kg i.p., prior- and post-treatment with a 24h interval before thioacetamide administrations) treated groups. RESULTS: : Thioacetamide administration caused hepatic damage creating oxidative and nitrosative stress accompanying perivenous necrosis and eosinophil infiltration. The significant elevation of total nitrite level in livers of thioacetamide treated groups reflected the activation of inducible nitric oxide synthase activity. The decrease in arginase activity indicated hepatic damage. Non-altered specific activity of arginase in the livers of thioacetamide treated groups did not overcome the elevation of NO production. Melatonin treatment did not modulate the levels/activities significantly. CONCLUSIONS: : Our results have indicated that nitrosative stress seems to be essentially critical in thioacetamide-induced hepatic failure in rats. Possible regulatory effect of arginase on NO production and applied dose of melatonin could not prevent hepatic damage.

Effect of congenital heart disease on renal function in childhood.

BACKGROUND: Nephropathy is a well-known complication of congenital heart disease (CHD), and the risk of developing renal impairment is particularly high in patients with cyanotic CHD. Most investigations of renal impairment in CHD have involved patients 20 years and older. This study investigated renal tubule function in pediatric patients with CHD, and compared findings in cyanotic and acyanotic groups. METHODS: Twenty children with acyanotic CHD, 23 children with cyanotic CHD, and 13 healthy children were enrolled. Blood and early morning urine samples were collected from each subject to measure urinary concentrations of sodium, microalbumin, creatinine, beta(2)-microglobulin, and N-acetyl-beta-D-glucosaminidase (NAG). RESULTS: The age and sex distributions in the three groups were similar. Median fractional excretion of sodium (FeNa) and urinary NAG/creatinine were significantly higher in the cyanotic group than in the control group (p = 0.022 and p = 0.002, respectively). There were no statistically significant differences among the groups with respect to urinary beta(2)-microglobulin/creatinine, urinary microalbumin/creatinine or glomerular filtration rate. CONCLUSION: Tubular injury can be detected before glomerular injury occurs even within the first decade of life in patients with cyanotic CHD.

Effect of iron deficiency anemia on renal tubular function in childhood.

Little is known about renal function in children with iron deficiency anemia. The purpose of this study was to investigate renal tubular function in these children. We compared renal tubular function in 20 children with iron deficiency anemia with 20 healthy age-matched controls. Blood and urine samples were obtained for hematological and biochemical analysis. Mean fractional excretion of sodium and mean urinary N-acetyl-beta- D-glucosaminidase/creatinine were significantly higher in the children with iron deficiency anemia than in controls (P<0.05). Hemoglobin levels were negatively correlated with urinary N-acetyl-beta- D-glucosaminidase/creatinine (r= -0.44, P=0.015), but were not correlated with fractional excretion of sodium (r= -0.29, P=0.13). There was no correlation between urinary N-acetyl-beta- D-glucosaminidase/creatinine and fractional excretion of sodium (r=0.32, P=0.09). The results suggest that children with iron deficiency anemia have impaired renal tubular function.