The Relationship of School Participation with Motor Proficiency and Executive Function in Children with Autism Spectrum Disorder

Abstract Objective participation in meaningful activities are important aspects of development in children with developmental disorder such as autism spectrum disorder. The purpose of this study was to assess the correlation of school participation with motor proficiency and executive function in children with Autism Spectrum Disorder. Materials & Methods In this cross-sectional (descriptive-analytic) study, 52 students aged 6 to 12 years old with ASD were selected through the convenience sampling method. The GARS-2 scale was used to confirm ASD diagnosis. Other psychiatric comorbidities such as ADHA were studied by the CSI-4 tool, and students with comorbidities were excluded. Data were collected using SFA, BOTMP-2, and BRIEF questionnaires. It should be noted that in the BRIEF questionnaire, a higher score indicates a more severe disability Results Our findings showed that motor proficiency and its components had a significant direct correlation with school participation in childrenwith ASD (P ≤0.001). On the other hand, school participation was inversely and significantly correlated with the behavioral regulation and metacognition monitoring indices of the executive function dimension (P <0.05). Conclusion Based on the findings of this research, the development of motor proficiency and improvements in the behavioral regulation andmetacognition monitoring of students with ASD will boost their participation in school activities. Motor proficiency was significantly correlated with school participation in children with ASD. More attention should be paid to perceptual motor interventions and cognitive rehabilitation programs (with a focus on monitoring metacognition and shifting behavioral regulation) to increase the participation of children with ASD in school activities

Antimicrobial efficacy of different concentration of sodium hypochlorite on the biofilm of Enterococcus faecalis at different stages of development

Persistent infection of the root canal due to the presence of resistance bacterial species, such as Enterococcus faecalis, has always been one of the most important reasons for endodontic treatment failure. This study investigated the antimicrobial efficacy of 1%, 2.5 % and 5% sodium hypochlorite in eliminating E. faecalis biofilms at different stages of development. In this study 4-, 6- and 10-week-old E. faecalis biofilms were subjected to one of the following approaches: phosphate-buffered saline solution (PBS) or 1%, 2.5% and 5% NaOCl. Dentin chip suspensions were used for colony forming unit (CFU) counting to estimate remaining E. faecalis counts. Statistical comparison of the means was carried out with Kruskal-Wallis test, and pair-wise comparisons were made by Mann-Whitney U test, at a significance level of P<0.05. The results showed that 2.5% and 5% NaOCl completely eliminated E. faecalis biofilms in three stages of biofilm development, whereas 1% NaOCl resulted in 85.73%, 81.88% and 78.62% decreases in bacterial counts in 4-, 6- and 10-week-old biofilms, respectively, which was significantly more than those with PBS (p<0.05). The bacteria in mature and old biofilms were more resistant to 1% NaOCl than were the bacteria in young biofilms. Overall survival rate and residual bacteria increased with biofilm aging

Aqua­chloridodimethyl­phenyltin(IV)–15-crown-5 (2/1)

The SnIV atom in the title compound, 2[Sn(CH3)2(C6H5)Cl(H2O)]·C10H20O5, exists in a trans-C3SnClO trigonal bipyramidal geometry in which the organo substituents occupy the equatorial sites. The coordinated water mol­ecule forms two hydrogen bonds to the 15-crown-5 mol­ecule, which is disordered about a center of inversion

1,5-Dichloro-4,8-dinitro­anthraquinone

The ring skeleton of the title compound, C14H4Cl2N2O6, is close to planar (r.m.s. deviation of the carbon atoms 0.091 Å); the nitro goups are twisted with respect to the mean plane of the ring system by 70.8 (1) and 86.7 (2)°. The crystal studied was found to be a merohedral twin, with a domain ratio of 0.61 (8):0.39 (8)

1,8-Dihydr­oxy-2,4,5,7-tetra­nitro-9,10-anthraquinone

The ring system in the title compound, C14H4N4O12, is essentially planar (r.m.s. deviation of the carbon atoms = 0.085 Å); the two hydr­oxy groups form intra­molecular hydrogen bonds to the same carbonyl O atom. The nitro groups are twisted with respect to the mean plane of the ring system by 74.3 (1) (1-nitro), 42.3 (3) (3-nitro), 45.7 (3) (6-nitro) and 66.9 (1)° (8-nitro)

1,5-Dicyano­anthraquinone

The complete mol­ecule of the title compound, C16H6N2O2, which is generated by a crystallographic inversion centre, is almost planar (r.m.s. deviation = 0.04 Å). In the crystal, adjacent mol­ecules are stacked along the a axis, with a shortest centroid–centroid separation of 3.826 (2) Å

Sumatriptan effects on morphine-induced antinociceptive tolerance and physical dependence: The role of nitric oxide

Sumatriptan, a 5HT (5-hydroxytryptamine)1B/1D receptor agonist, showed neuroprotection in different studies. The aim of the present study was to investigate the effect of sumatriptan on morphine-induced antinociceptive tolerance and physical dependence. We also investigated the possible role of nitric oxide (NO) on sumatriptan effects. Tolerance was induced by morphine injection (50, 50, 75 mg/kg) three times daily for five days. Antinociceptive latency after acute and chronic treatment with sumatriptan (0.001, 0.01, 0.1 and 1 mg/kg) was measured by hot plate test in morphine-dependent animals. To investigate the possible involvement of NO, different isoforms of nitric oxide synthase (NOS) inhibitors including L-NAME, aminoguanidine and 7-nitroindazole were co-administered with sumatriptan. Nitrite level in mice hippocampus was quantified by Griess method. To examine the role of sumatriptan on physical dependence, three parameters of withdrawal signs were recorded after injection of naloxone (4 mg/kg). Acute treatment with sumatriptan (0.01, 0.1 and 1 mg/kg) attenuated the antinociceptive tolerance (P < 0.001). Chronic injection of sumatriptan (0.001, 0.01 and 0.1 mg/kg), as well, decreased the antinociceptive tolerance (P < 0.001). Moreover, co-administration of NOS inhibitors prevented the effects of sumatriptan. Sumatriptan significantly increased the level of nitrite only after chronic administration. Sumatriptan administration showed no alteration in naloxone-precipitated withdrawal signs. Acute and chronic administration of sumatriptan attenuated morphine antinociceptive tolerance; at least in chronic phase via nitrergic pathway. Our data did not support beneficial effects of sumatriptan on morphineinduced physical dependence in mice

Anticonvulsant effect of minocycline on pentylenetetrazole-induced seizure in mice: involvement of nitric oxide and N-methyl-D-aspartate receptor

Anticonvulsant effects of minocycline have been explored recently. This study was designed to examine the anticonvulsant effect of acute administration of minocycline on pentylenetetrazole-induced seizures in mouse considering the possible role of the nitric oxide/N-methyl-D-aspartate (NMDA) pathway. We induced seizure using intravenous administration of pentylenetetrazole. Our results showed that acute administration of minocycline increased the seizure threshold. Furthermore, co-administration of subeffective doses of the nonselective nitric oxide synthase (NOS) inhibitor NG-L-arginine methyl ester (10 mg/kg) and the neuronal NOS inhibitor 7-nitroindazole (40 mg/kg) enhanced the anticonvulsant effect of subeffective doses of minocycline (40 mg/kg). We found that inducible NOS inhibitor aminoguanidine (100 mg/kg) had no effect on the antiseizure effect of minocycline. Moreover, L-arginine (60 mg/kg), as a NOS substrate, reduced the anticonvulsant effect of minocycline. We also demonstrated that pretreatment with the NMDAreceptor antagonists ketamine (0.5 mg/kg) and MK-801 (0.05 mg/kg) increased the anticonvulsant effect of subeffective doses of minocycline. Results showed that minocycline significantly decreased the hippocampal nitrite level. Furthermore, co-administration of a neuronal NOS inhibitor like NMDA receptor antagonists augmented the effect of minocycline on the hippocampal nitrite level. In conclusion, we revealed that anticonvulsant effect of minocycline might be, at least in part, due to a decline in constitutive hippocampal nitric oxide activity as well as inhibition of NMDA receptors

Experiencing neonatal maternal separation increased the seizure threshold in adult male mice: Involvement of the opioid system

Experiencing early-life stress has been considered as a potent risk factor for the development of many of brain disorders, including seizures. Intervening mechanisms through which neonatal maternal separation (MS) alters the seizure susceptibility in adulthood have not been well studied. In the current study, by applying 180 min of MS stress (PND 2–14), we determined the seizure susceptibility and considered the role of the opioid system. Maternal separation increased the seizure threshold, and administration of anticonvulsant/proconvulsant doses of morphine (1 and 30 mg/kg, respectively) reversed the impact of MS. Using tail flick and hot plate tests, we exposed animals to 30 min Restraint stress (RS) and found that MS decreased the pain threshold, suggesting the hyporesponsiveness of the opioid system. These results supported the abnormal seizure activity observed in the MS mice and suggested that abnormalities in the opioid system following MS alter seizure susceptibility in later life

Morphine modulates the effects of histamine H1 and H3 receptors on seizure susceptibility in pentylenetetrazole-induced seizure model of mice

Histamine regulates release of neurotransmitters such as dopamine, serotonin, gamma-aminobutyric acid (GABA), glutamate and also is involved in several functions in central nervous system (CNS). It has been shown that histamine participates in disorders like seizure. It has been well documented that morphine dose-dependently induces anti or proconvulsant effects. In the current study, we firstly showed that morphine (1 mg/kg) exerts anticonvulsant effects which significantly reversed by naltrexone administration. Secondly, we determined seizure threshold for H1 and H3 receptors agonists and antagonists in mouse model of pentylenetetrazole (PTZ)-induced clonic seizures. Our results showed that activation of H1 receptors by 2-(2-Pyridyl)-ethylamine exerts anticonvulsant properties while inhibition of H1 receptors by pyrilamine maleate induced proconvulsant effects. Furthermore, we showed that immepip dihydrobromide, a H3 receptor agonist, increased seizure susceptibility to PTZ whereas thioperamide, a H3 receptor antagonist increased seizure threshold. We also revealed that pretreatment with morphine potently reversed the effects of histaminergic system on seizure threshold suggesting the involvement of opioid system in alteration of seizure threshold by histaminergic drug