The prevalence of features of attention deficit hyperactivity disorder in a special school in Ireland

Background The prevalence of features of attention deficit hyperactivity disorder (ADHD) in children with intellectual disabilities (ID) in Irish schools is unknown. The aim of this study was to examine the prevalence of features of ADHD in a special school, in order to ascertain the number of children who may need further assessment for ADHD. The study also explores the reliability of the Conners Teachers Rating Scale in this population. Method All teachers in a special school for children with ID were asked to complete the Conners Teachers Rating Scale and the Attention‐Distractibility, Inhibition–Excitation Classroom Assessment Rating Scale, for those children whose parents had consented for them to take part in this study. Consent was obtained for 84 children a response rate of 71%, between the ages of 5 and 18 (mean = 10.5 years; SD = 3.7). Results The Conners Teachers Rating Scale was found to be internally reliable and had a normal distribution with our results. Overall, 55.9% of participants (47/84) had markedly elevated scores (T > 69) for at least one of the target subscales, which were the ‘Hyperactivity’, ‘Inattention’ and the ‘ADHD Index’ subscales of the Conners Teachers Rating Scales. In addition, the findings would suggest that the Conners Teachers Rating Scale can be a useful screening tool in the population of school children with ID. Conclusions The study suggests that ADHD may be under diagnosed in children with ID. This has practical implications for the mental health needs of these children. It is recommended that further studies are carried out to determine the prevalence of ADHD in this population.     

Histopathology of experimentally induced asthma in a murine model of sickle cell disease

Asthma is a comorbid condition associated with increased rates of pain, acute chest syndrome, and premature death in human sickle cell disease (SCD). We developed an experimental asthma model in SCD and control mice expressing either normal human or murine hemoglobin to determine its effect on mortality and lung pathology. To induce lung inflammation, experimental mice were sensitized to ovalbumin (OVA) by subcutaneous OVA implantation (Sen), allowed 2 weeks to recover, and then divided into 2 groups, each receiving over a subsequent 10-day period the same dosage of aerosolized OVA but 2 different levels of exposure: 15 minutes (LoSen) and 30 minutes (HiSen). During recovery, 10% of SCD mice died compared with no deaths in control mice. An additional 30% of HiSen SCD mice died during aerosolization compared with 10% in LoSen SCD. Histologic indices of lung inflammation (eg, eosinophil recruitment, airway and vessel wall thickening, and immunoreactive TGFbeta and fsp-1) and bronchial alveolar lavage fluid eosinophil peroxidase activity differentially increased in sensitized mice compared with unsensitized mice. Our findings indicate SCD mice with experimentally induced asthma are more susceptible to death and pulmonary inflammation compared with control mice, suggesting that asthma contributes significantly to morbidity and mortality in SCD.     

Influenza in pregnancy

Please cite this paper as: Memoli et al. (2012) Influenza in pregnancy. Influenza and Other Respiratory Viruses 00(00), 000–000.The 2009 pandemic served as a strong reminder that influenza‐induced disease can have a great impact on certain at‐risk populations and that pregnant women are one such important population. The increased risk of fatal and severe disease in these women was appreciated more than 500 years ago, and during the last century, pregnant women and their newborns have continued to be greatly affected by both seasonal and pandemic influenza. In this review, we briefly discuss the data collected both before and after the 2009 pandemic as it relates to the impact of influenza on pregnant women and their fetuses/newborns, as well as risk variables, clinical features, clues to pathophysiologic mechanisms, and approaches to treatment and prevention.     

Different immunological sensitizing regimens and airway responsiveness in vitro to contractile agonists in guinea-pigs

Groups of guinea-pigs were sensitized to ovalbumin, using different regimens to induce either IgG-like antibodies or IgE-like and IgG-like antibodies and the responsiveness to histamine and carbachol in vitro of tracheal and lung parenchymal strips was determined. EC50 values for histamine and carbachol in both tracheal and lung parenchymal strips were not significantly different for either group of sensitized guinea-pigs or their respective controls. The maximal tension developed in parenchymal strips was not significantly different for either sensitized or control groups. For tracheal strips, maximal tension was not significantly different in each group except in animals with IgG-like antibodies, which developed less maximal tension with histamine than controls. The absence of any increase in maximal tension or any change in EC50 to histamine or to carbachol in tracheal or parenchymal strips from immunized guinea-pigs indicates that immunological sensitization does not increase the responsiveness of smooth muscle to these contractile agonists.     

Synthesis, pharmacological action, and receptor binding affinity of the enantiomeric 1-(1-phenyl-3-methylcyclohexyl)piperidines

The cis and trans enantiomers of the 1-(1-methylcyclohexyl)piperidines were prepared from either 3(R)- or 3(S)-methylcyclohexanone through the Bruylents reaction or a modified azide route, respectively. Separation of the intermediate amines 5 and 6 was achieved through chromatography or selective crystallization of a fumarate salt. The cis isomer 2b had about one-third of the affinity of phencyclidine for the PCP receptor. The other isomers were less potent. There was a 40-fold difference between the binding affinity of the cis enantiomers 2a and 2b and a fourfold difference between the affinities of the trans enantiomers 1a and 1b. None of the compounds antagonized the stereotypy induced by phencyclidine in the rotorod assay in mice, after intraperitoneal introduction.     

A calcium channel mutant mouse model of hypokalemic periodic paralysis

Hypokalemic periodic paralysis (HypoPP) is a familial skeletal muscle disorder that presents with recurrent episodes of severe weakness lasting hours to days associated with reduced serum potassium (K⁺). HypoPP is genetically heterogeneous, with missense mutations of a calcium channel (Ca_V1.1) or a sodium channel (Na_V1.4) accounting for 60% and 20% of cases, respectively. The mechanistic link between Ca_V1.1 mutations and the ictal loss of muscle excitability during an attack of weakness in HypoPP is unknown. To address this question, we developed a mouse model for HypoPP with a targeted Ca_V1.1 R528H mutation. The Ca_v1.1 R528H mice had a HypoPP phenotype for which low K⁺ challenge produced a paradoxical depolarization of the resting potential, loss of muscle excitability, and weakness. A vacuolar myopathy with dilated transverse tubules and disruption of the triad junctions impaired Ca²⁺ release and likely contributed to the mild permanent weakness. Fibers from the Ca_V1.1 R528H mouse had a small anomalous inward current at the resting potential, similar to our observations in the Na_V1.4 R669H HypoPP mouse model. This “gating pore current” may be a common mechanism for paradoxical depolarization and susceptibility to HypoPP arising from missense mutations in the S4 voltage sensor of either calcium or sodium channels.