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Biomedical subjects

M Akisu

Publications and source records attributed to M Akisu.

10 recordsLinked to original sources

Supplementation with Saccharomyces boulardii ameliorates hypoxia/reoxygenation-induced necrotizing enterocolitis in young mice.

Intestinal bacterial proliferation is an important aspect of gastrointestinal injury in neonatal necrotizing enterocolitis (NEC). In the present investigation, we examined the protective action of oral supplementation with Saccharomyces boulardii (S. boulardii), non-pathogen probiotic yeast, against hypoxia-reoxygenation (H/R)-induced NEC in young mice. Young mice were divided into three groups; Group 1 mice (untreated) were subjected only to hypoxia-reoxygenation; Group 2 mice were subjected to hypoxia-reoxygenation and were then given lyophilized S. boulardii (10 mg suspended in 0.5 ml saline) twice a day by orogastric intubation for 10 days. Group 3 mice served as controls. Hypoxia was induced by placing young mice in a 100 % CO (2) chamber for 5 min. After hypoxia, the young mice were reoxygenated for 10 min with 100 % oxygen. We examined the intestinal lesions by light microscopy and measured intestinal generation of PAF and TNF-alpha in the H/R-induced model of NEC. In the probiotic group, NEC-induced intestinal tissue damage was greatly attenuated, with necrosis partially limited to the mucosa. Both intestinal tissue PAF and TNF-alpha concentrations were significantly higher in the untreated group than in controls (p < 0.001). S. boulardii-supplemented young mice showed a significant decrease in intestinal generation of PAF compared with untreated young mice (p < 0.05). On the other hand, no significant difference was observed in the intestinal concentration of TNF-alpha between untreated and probiotic groups ( p > 0.05). The present study suggests that hypoxia/reoxygenation plays an important role in the pathogenesis of NEC and supports hypothesis that especially PAF and TNF-alpha are involved in the pathophysiological mechanism of H/R-induced NEC. This study also demonstrates that dietary supplementation with S. boulardii ameliorates the histologic evidence of H/R-induced intestinal injury. Based on these findings, the beneficial effects of probiotic S. boulardii in this model of NEC are mediated via mechanisms inhibiting intestinal proinflammatory mediator release.

Animals↗

Transient fetal myelosuppressive effect of D-penicillamine when used in pregnancy.

Normal fertility is sustained by progress in the medical therapy of Wilson's disease; however, pregnancy complications are encountered more frequently. The mother we present is a Wilson's disease patient who had been compliant with D-penicillamine for the preceding 13 years. She was admitted with unplanned pregnancy at the 16th gestational week. The dose of D-penicillamine could be reduced to 600 mg/d related to the underlying disease. Pregnancy ended with premature labor and delivery at the 29-30th weeks. The baby experienced type I respiratory distress and was treated by surfactant and mechanical ventilation. Neutropenia and leucopenia were documented at 6th postnatal hours. The baby showed neutropenia and leucopenia for 5 days and resolving without any further therapy. Intrauterine D-penicillamine was suspected to cause transient neonatal myelosuppression.

Chelating Agents↗

The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the generation of platelet-activating factor and leukotriene B4 in hypoxic-ischemic brain in young mice.

Platelet-activating factor (PAF), leukotriene B(4) (LTB(4)) and other cytokines have been indicated to be responsible for the neuronal damage in hypoxic-ischemic brain. Diets in omega-3 (n-3) fatty acids appear to have an antiinflammatory effect, which is thought to be due to decrease in active prostaglandins and leukotrienes production after incorporation of these fatty acids into cell membrane phospholipids. We investigated the effect of dietary supplementation with n-3 fatty acids on endogenous PAF and LTB(4) biosynthesis in hypoxic-ischemic brain of young mice. Young mice were randomly divided into four groups: Group 1 mice were fed standard chow (n-3 polyunsaturated fatty acids free); Group 2 and Group 3 mice were given standard diet supplemented with 10% by weight of fish oil, as source of n-3 polyunsaturated fatty acids, for 3 and 6 weeks, respectively. Group 4 mice served as control. We injured the right cerebral hemisphere of young mice by ligating the right common carotid artery and exposing the mice to 8% oxygen for 60 min. Approximately 10-fold increase in PAF concentration was determined in hypoxic-ischemic brain tissue of Group 1 mice. Tissue concentration of PAF showed a profound decline in Group 3 mice compared to Groups 1 and 2 (P<0.01, P<0.05, respectively). LTB(4) was also significantly elevated in the brain of Group 1 mice when compared to the brain of control mice (P<0.001). A striking decline was observed in the concentration of LTB(4) in both Group 2 and Group 3 mice compared to Group 1 mice (P<0.05, P<0.01, respectively). The present study shows that n-3 fatty-acid-enriched diet inhibits endogenous PAF and LTB(4) generation in hypoxic-ischemic brain tissue; however it demonstrates that 6 weeks of dietary supplementation with n-3 fatty acids results in a significant decrease in tissue level of PAF in the brain.

Animals↗

Molybdenum cofactor deficiency associated with Dandy-Walker complex.

Molybdenum cofactor deficiency is a rare and devastating disease leading to intractable seizures in the neonatal period. Severe loss of neocortical neurons, gliosis, and cystic necrosis of cerebral white matter resulting in significant cerebral volume loss are the neuropathological findings. The mechanism of cerebral injury is unknown, but sulphite excess, and sulphate or uric acid deficiencies are possible factors. We present here a new case of Molybdenum cofactor deficiency associated with Dandy-Walker complex with a history of three dead siblings, the latter also having Dandy-Walker malformation. We speculate that severe cerebral volume loss due to the above mentioned mechanisms may lead to an appearance resembling Dandy-Walker malformation.

Brain↗

The role of recombinant human erythropoietin in lipid peroxidation and platelet-activating factor generation in a rat model of necrotizing enterocolitis.

In the present study we examined the effect of recombinant human erythropoietin (rhEPO) on intestinal malondialdehyde (MDA) as an index of lipid peroxidation, related to iron-catalysed free radical reaction and platelet-activating factor (PAF) synthesis in the experimental model of necrotizing enterocolitis (NEC). Three groups, each consisting of eight 1-day-old Wistar albino rat pups, were studied; Group 1, hypoxia-reoxygenation; Group 2, hypoxia-reoxygenation and rhEPO pretreatment; Group 3, control. rhEPO was given 750 U/kg/week by intraperitoneal injection three times a week for 2 weeks. On day 15th of life, hypoxia was induced by placing rat pups in a 100% CO2 chamber for 5 min. After hypoxia, the rat pups were reoxygenated for 10 min with 100% oxygen and returned to their mothers. All pups were killed at 4h following hypoxia-reoxygenation. The abdomen was opened and representative samples of injured areas were taken for histopathologic examination. MDA and PAF levels were determined in the intestine. Significantly increased intestinal MDA content was found in Group 1 rat pups compared to Group 2 and Group 3 pups (p < 0.001 and p < 0.001, respectively). However, PAF concentrations were highly elevated in the intestine of Group 1 and Group 2 pups (p>0.05) when compared to the intestine of Group 3 pups (p < 0.001 and p < 0.001, respectively). Histopathologic findings did not differ between Groups 1 and 2. The present study demonstrates that oxygen-derived free radicals and PAF are involved in the pathophysiological mechanism of the development of NEC. This study also shows that administration of rhEPO significantly decreases lipid peroxidation; however, PAF generation was not inhibited in hypoxia-induced bowel necrosis.

Animals↗

Effect of recombinant human erythropoietin administration on lipid peroxidation and antioxidant enzyme(s) activities in preterm infants.

In the present investigation, we studied the effect of recombinant human erythropoietin (r-HuEPO) on serum malondialdehyde (MDA) as an index of lipid peroxidation, related to iron-catalyzed free radical reaction and erythrocyte superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities in very-low-birth weight (VLBW) infants. Forty premature infants, at gestational ages were less than 33 weeks and birthweights were less than 1,500 g, were enrolled in the study. The study population was randomly divided into 2 groups. Twenty infants in Group 1 (treatment group) were given r-HuEPO, and 20 infants in Group 2 served as the control. r-HuEPO treatment (750 U/kg a week) was initiated on the 10th day of life and continued for 6 weeks. Preterm infants given erythrocyte transfusions during the study were excluded from the results. Serum ferritin and MDA levels, and erythrocyte superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities were analyzed at the end of the first week of life (at the beginning of the study). Subsequently, serum ferritin, and MDA levels were measured at the end of the 3rd and the 6th week. SOD, CAT, and GPX activities in the hemolysate were analyzed at the end of the 4th week. Six infants in the control group and 1 infant in the r-HuEPO group received transfusions through the end of the study, and these infants were excluded from the results. Significantly decreased serum ferritin concentrations were found in the r-HuEPO group compared to those in the control group both at the end of the 3rd and the 6th week (P < 0.05, and P < 0.01, respectively). In addition, serum MDA levels were also significantly reduced in Group 1 compared to control both at the end of the 3rd and the 6th week (P < 0.01 and P < 0.05, respectively). A good correlation was found between serum MDA and ferritin levels in Group 1. When the 2 groups were compared with respect to activities of SOD, CAT, and GPX at the end of the 4th week, no differences were observed. Our findings in this study show that administration of r-HuEPO significantly decreases lipid peroxidation, but does not affect erythrocyte antioxidant enzyme(s) activities in preterm infants. The mechanism responsible for the r-HuEPO-induced decrease in lipid peroxidation may concern inhibition to iron-catalyzed free radical reactions.

Aging↗

A comparison of efficacy between two natural exogenous surfactant preparations in premature infants with respiratory distress syndrome.

The mortality and various morbidity rates have been substantially reduced by means of exogenous surfactant replacement, the cornerstone in the treatment of respiratory distress syndrome (RDS) in premature infants. The objective of this study is to compare two natural surfactant preparations (Alveofact(R), Survanta(R)) in terms of effectiveness and side-effects. A total of 50 infants with RDS were given surfactant due to RDS were taken into the scope of this study. Survanta(R) and Alveofact(R) were administered to randomized infants with RDS and the results obtained during clinical observations were compared. Second hour mean FiO (2), MAP and a/APO (2) values showed changes in favour of Alveofact(R) (n = 25) group compared to the Survanta(R) (n = 25) group (p < 0.05 for each parameter). However, this difference disappeared in the 6 (th) hour. No statistical difference was established between the two groups with regard to sideeffects (pneumothorax, sepsis, intraventricular hemorrhage, bronchopulmonary dysplasia), duration of mechanical ventilation in survivors, duration of hospitalization in survivors and mortality before the 28 (th) day. It was concluded that results obtained with different surfactant preparations having dissimilar compositions were not different in terms of final impacts and side-effects.

Biological Products↗

Experience with teicoplanin in the treatment of neonatal staphylococcal sepsis.

We aimed to evaluate retrospectively the clinical and bacteriological efficacy and potential side-effects of teicoplanin treatment in neonates with proven staphylococcal infection. There were 37 episodes of staphylococcal septicaemia in neonates with a mean gestational age of 34.2 +/- 2.3 weeks; 26 were caused by coagulase-negative staphylococcal (CoNS) sepsis and 11 by Staphylococcus aureus sepsis. All episodes were treated with teicoplanin (intravenous loading dose 16 mg/kg followed by a maintenance dose of 8 mg/kg daily). The methicillin resistance and antibiotic susceptibilities of both micro-organisms were evaluated. Bacterial eradication was achieved in 89.1% of cases and mortality was 16.2%. The mean duration of treatment of the survivors was 11.6 +/- 2.3 days. There were no drug-related adverse events and the biochemical and haematological tests showed no clinically significant changes in relation to teicoplanin therapy. Our results suggest that teicoplanin is highly effective in neonatal staphylococcal sepsis.

Anti-Bacterial Agents↗