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Neuroprotective effect of levetiracetam on hypoxic ischemic brain injury in neonatal rats

PurposeHypoxic-ischemic brain injury that occurs in the perinatal period is one of the leading causes of mental retardation, visual and auditory impairment, motor defects, epilepsy, cerebral palsy, and death in neonates. The severity of apoptosis that develops after ischemic hypoxia and reperfusion is an indication of brain injury. Thus, it may be possible to prevent or reduce injury with treatments that can be given before the reperfusion period following hypoxia and ischemia. Levetiracetam is a new-generation antiepileptic drug that has begun to be used in the treatment of epilepsy.MethodsThe present study investigated the effects of levetiracetam on neuronal apoptosis with histopathological and biochemical tests in the early period and behavioral experiments in the late period.ResultsThis study showed histopathologically that levetiracetam reduces the number of apoptotic neurons and has a neuroprotective effect in a neonatal rat model of hypoxic-ischemic brain injury in the early period. On the other hand, we demonstrated that levetiracetam dose dependently improves behavioral performance in the late period.ConclusionsBased on these results, we believe that one mechanism of levetiracetam’s neuroprotective effects is due to increases in glutathione peroxidase and superoxide dismutase enzyme levels. To the best of our knowledge, this study is the first to show the neuroprotective effects of levetiracetam in a neonatal rat model of hypoxic-ischemic brain injury using histopathological, biochemical, and late-period behavioral experiments within the same experimental group.

Mesenchymal stem cell treatment in hyperoxia-induced lung injury in newborn rats.

The aim of this study was to evaluate the effectiveness of tracheally delivered mesenchymal stem cells (MSC) on lung pathology in a hyperoxia‐induced lung injury (HILI) model in neonatal rats.

Comparison of selective head cooling versus whole-body cooling

This study compared selective head cooling (SHC) and whole‐body cooling (WBC) in newborns with hypoxic–ischemic encephalopathy (HIE).

A rare case of cardiac anomaly: prenatally diagnosed ectopia cordis.

Ectopia cordis is a rare congenital malformation in which the heart is located partially or totally outside the thoracic cavity. The estimated prevalence of ectopia cordis is 5.5-7.9 per million births and it comprises 0.1% of congenital heart diseases. Ectopia cordis is associated with other congenital heart diseases and various tissue and organ disorders. Common cardiac anomalies associated with ectopia cordis include ventricular septal defect, atrial septal defect, pulmonary stenosis, right ventricular diverticulum, double right ventricular outflow tract and tetralogy of Fallot. Extracardiac anomalies associated with ectopia cordis reported in the literature include omphalocele, gastrochisis, cleft lip and palate, scollosis and central nervous system malformations. Here we report a newborn with ectopia cordis who was diagnosed prenatally.

The effects of fibroblast growth factor-2 and pluripotent astrocytic stem cells on cognitive function in a rat model of neonatal hypoxic-ischemic brain injury.

Abstract Objective: This study aimed to determine the effect of pluripotent astrocytic stem cells (PASCs) and fibroblast growth factor-2 (FGF-2) on cognitive function in neonatal rats with hypoxic-ischemic brain injury (HIBI). Methods: The study was performed on 7-d-old rats that were randomly divided into four groups. All rats, except those in the sham group, were kept in a hypoxic chamber containing 8% oxygen for 2 h after the ligation of the right carotid artery. Next, 5 d after HIBI was induced, PASCs were administered to the motor cortex, and FGF-2 was administered intraperitoneally to group AF; PASCs were administered to the motor cortex, and salt solution buffered with phosphate was administered intraperitoneally to group A; and fresh cell culture solution (medium) was administered to group M. Immunofluorescence was used to localize the administered PASCs in the brains of rats from groups A and AF. The Morris water maze tank (MWM) test was performed to assess the rats’ cognitive functions at week 12. The rats that were administered PASCs were observed for the development of neoplasms and autopsies were performed after 30 months. Results: PASCs migrated to damaged brain regions surrounding the hippocampus in groups A and AF. The mean platform finding time (PFT) significantly decreased over time in each group on day 1–4 of MWM testing (p < 0.001). On day 2–4, the mean PFT was shortest in group S followed by group AF. In group A, the PFT was significantly longer than in group S on day 3–4 (p = 0.01 and 0.007, respectively). On day 5 of the MWM test, the time spent in the eastern quadrant (which previously contained the platform) was longest in group S followed by groups AF, A, and M; however, the differences between groups were not significant (p = 0.51). After 30 months, none of the rats in groups A or AF had benign or malignant neoplasms. Conclusions: Following the administration of PASCs in rats with experimentally induced HIBI, PASCs migrated to the injured brain regions; however, treatment with PASCs did not have a positive effect on cognitive function. The administration of FGF-2 together with PASCs resulted in positive cognitive results, although not at the level of significance.

A case of thanatophoric dysplasia type 2: a novel mutation.

Thanatophoric dysplasia (TD) is a lethal form of skeletal dysplasia with short-limb dwarfism. Two types distinguished with their radiological characteristics have been defined clinically. The femur is curved in type 1, while it is straight in type 2. TD is known to be due to a mutation in the fibroblast growth factor receptor 3 (FGFR3) gene. We report a male patient who showed clinical findings congruent with TD type 2 and a new mutation in the FGFR3 gene, a finding which has not been reported previously.

Bone age and probable aetiological causes in primary nocturnal enuresis.

Aim: To investigate probable aetiological risk factors and to identify whether there are any differences in bone age between normal children and children with primary nocturnal enuresis (PNE). Methods: Ninety children with primary nocturnal enuresis and 40 healthy children were included in the study. Enrolment began in January 2001, and continued through July 2002. Data were obtained via consultation with children and their families, physical examination and laboratory findings. Left hand and wrist graphs of each patient were acquired, and, using Tanner Whitehouse charts (TW‐2), bone ages were determined via comparison of 20 hand and wrist bones. Results: Of the total of 90 children with primary nocturnal enuresis participating in the study, 52 (57.8%) were male and 38 (42.2%) were female. Of the control group, 24 (60%) were male and 16 (40%) were female. Differences between chronological ages and bone ages of the PNE and control groups were 0.57±0.59 and 0.54±0.67 y, respectively, and no significant difference was seen (p=0.484). In 90% of the children in the PNE group there was found to be a primary nocturnal enuresis history in the family, whereas in the control group this rate was only 7.5%. Of the children with PNE, 62.2% had very deep sleeping habits, while 7.5% of the control group had this problem.

Lethal neonatal rigidity and multifocal seizure syndrome with a new mutation in BRAT1

Rigidity and Multifocal Seizure Syndrome, Lethal Neonatal (RMFSL) (OMIM# 614498) is a rare and recently characterized epileptic encephalopathy that is related to variants in the BRAT1 gene (Breast Cancer 1-associated ataxia telangiectasia mutated activation-1 protein). In this report, an RMFSL case, who died in the 10th month of the life, with rigidity, drug-resistant myoclonic seizures in the face and extremities, with, significant motor delays is presented. The exon sequence was determined and a new homozygous variant (C.2230_2237dupAACATGC) was detected. This RMFSL case with a homozygous variant in the BRAT1 gene, is the fourth one in the literature and the first one being reported from a Turkish family.

Is levetiracetam neuroprotective in neonatal rats with hypoxic ischemic brain injury

BACKGROUND The aim of this study was to determine if levetiracetam (LEV) is neuroprotective in neonatal rats with hypoxic-ischemic brain injury (HIBI). METHODS The study included 7-d-old male Wistar rats that were randomly divided into the LEV400, LEV800, control, and sham groups. All the rats, except those in the sham group, underwent ligation of the carotid artery and were then kept in a hypoxic chamber containing 8% oxygen for 2 h. At the end of the hypoxic period the rats in the control group were administered saline solution 0.5 mL, the rats in the LEV400 group were administered LEV 400 mg.kg-1, and rats in the LEV800 group were administered LEV 800 mg.kg-1 via the intraperitoneal route. The terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) method was used to evaluate neuronal apoptosis in the rats. The Morris Water Maze (MWM) test was performed at age 14 weeks in order to evaluate cognitive function. RESULTS The number of apoptotic neurons in the right hemispheres was significantly lower in the sham, LEV400, and LEV800 groups than in the control group (p < 0.001, p < 0.001, and p < 0.001, respectively). In addition, the number of apoptotic neurons in the right hemispheres was significantly lower in the LEV800 group than in the LEV400 group (p = 0.001). Platform finding time (PFT) during MWM testing was significantly shorter in the sham and LEV800 groups on d 4 than on d 1 (p = 0.001 and p = 0.006, respectively); however, PFT did not significantly change between d 1 and d 4 in the control or LEV400 groups (p = 0.91 and p = 0.096, respectively). CONCLUSION Based on the present findings, LEV exhibited a dose-dependent neuroprotective effect in neonatal rats with HIBI (Ref. 27).

Evaluation of Score for Neonatal Acute Physiology and Perinatal Extension II and Clinical Risk Index for Babies with additional parameters

The aim of this study was to determine mortality risk by calculating Score for Neonatal Acute Physiology and Perinatal Extension II (SNAP‐PE‐II) and Clinical Risk Index for Babies (CRIB) score, and evaluate prediction of the effects of antenatal corticosteroid and surfactant treatment on mortality.