The purpose of this study was to investigate the possible association between childhood epilepsy and KCNJ10 gene polymorphisms (rs61822012 and rs2486253). A total of 200 epileptic cases and 200 healthy controls enrolled to this study. Genomic DNAs from the patients and control cases were analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism methods. There were significant associations between the G/T genotype of KCNJ10 gene rs2486253 polymorphism in the idiopathic generalized epilepsy group (P = .037) and in subjects with generalized tonic-clonic seizures (P = .0015). T allele was also increased in patients with generalized tonic-clonic seizures (P = .0158). However, no statistically significant association was found between rs61822012 polymorphism and epilepsy. Our data suggest that G/T genotype of the KCNJ10 gene rs2486253 polymorphism affects risk for development of common types of childhood epilepsy. The T allele of this polymorphism was found to be a seizure-susceptibility allele for tonic-clonic epilepsy.

Background:: Lung and breast cancer are the most frequent causes of death from cancer globally. The objectives of this research were to evaluate the serum mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) and humanin levels in lung or breast cancer patients, and investigate the impacts of radiation therapy on the circulating levels of these peptides. Methods:: 35 lung cancer patients, 34 breast cancer patients, and healthy volunteers as a control group were recruited in this prospective observatory research. Lung cancer patients with stage IIIA/IIIB were treated with paclitaxel-based chemotherapy plus radiotherapy (2 Gy per day, 30 times, 60 Gy total dose). Breast cancer stage IIA/IIB patients were treated with postoperative locoregional radiation therapy (2 Gy per day, 25 times, 50 Gy total dose). The ELISA method was used to detect serum humanin and MOTS-c levels during, before, and after radiotherapy. Results:: We observed marked elevations in circulating MOTS-c, but not humanin levels in patients with lung cancer (P < 0.001). Radiation therapy led to a marked augmentation in MOTS-c levels in these patients (P < 0.001). On the other hand, there was a marked decline in humanin, but not MOTS-c, levels in breast cancer patients (P < 0.001). Conclusion:: Our research has shown, for the first time, that increased MOTS-c and decreased humanin levels play a role in lung cancer and breast cancer, respectively. Additionally, radiotherapy modifies MOTS-c levels in patients with lung, but not breast cancer.

Breath-holding spells (BHS) are common nonepileptic paroxysmal events in children. This is a retrospective study to compare the effectiveness of oral theophylline, piracetam, and iron treatments in children with simple BHS. A total of 146 children (75 girls and 71 boys) with simple BHS were included to this retrospective study. Children were divided into 4 groups: nontreated (no anemia and no treatment), oral theophylline (10 mg/kg/d as a single daily dose), piracetam (40 mg/kg/d in 2 divided doses), and elementary iron (3 mg/kg/d as a single daily dose) treatments. Iron therapy had been given only in children with iron deficiency anemia. Neurologic, cardiologic, and biochemical evaluations were performed for all children. The majority of the patients had cyanotic spells (83.6%). The frequency of attacks/month was markedly decreased with iron (58.8%) and theophylline (82.9%) treatments, but not with piracetam therapy (8.8%) and nontreated group (4.7%). Satisfaction of the parents/caregivers was found to be high in the theophylline group (P < .001). Our results showed that theophylline was the most effective therapy to decrease the frequency of simple BHS in children.

Recent studies suggest that ischemic preconditioning (IP) of the lung may have a protective effect in ischemia-reperfusion (I/R) injury. The purpose of the present study was to investigate the preconditioning hypothesis in rat pulmonary vascular bed and to examine the role of nitric oxide (NO) in IP. Isolated rat lung was perfused with Krebs-Henseleit solution containing indomethacin at a constant flow rate and perfusion pressure changes was recorded by a pressure transducer. In rat pulmonary vascular bed, 2 hours of hypothermic ischemia significantly attenuated histamine-induced vasodilator responses without affecting sodium nitroprusside (SNP) vasodilation when compared to sham values. However, 2 cycles of 5 minutes of ischemia and reperfusion that were applied prior to 2 hours of ischemia (IP protocol) prevented the attenuation of histamine-induced vasodilation. On the other hand, IP failed to prevent pulmonary edema after ischemia. Histopathological examination of rat lungs demonstrated that IP was able to protect endothelial cells and type II pneumocytes in lung. Moreover, in IP group, malondialdehyde (MDA) contents of the lung tissue were significantly lower and tissue glutathione (GSH) contents were significantly higher than those in I/R group. Administration of NO synthase inhibitor, N^G-nitro-L-arginine-methyl ester (L-NAME) prior to the IP protocol abolished the protective effects of IP, but not affected the tissue malondialdehyde and glutathione levels. These results suggest that I/R impaired endothelium-dependent vasodilatory response, whereas endothelium-independent SNP-induced responses were preserved in rat pulmonary vascular bed. IP prevented the impairment of pulmonary vascular endothelium-dependent responses, and these effects may be partially mediated by NO.