Singing disability in school children

In an effort to discover the cause of, and a cure for singing disability, seventy-nice children and two adults were observed and given treatment between 1939 and the present time. Fifty of them were given various tests to this end, records being kept. Fifty-three were cured, five left the district, fifteen are still having lessons, and eight were improved but not cured, though it now seems that they might have been. The main cause was slower learning than normal, due to the absence of singing at home, or a lack of interest which often went with lower musical intelligence. Slower learning, as a rule only presented difficulty where it had been the subject of comment or criticism, and where the child had not been allowed to try to sing. The mental attitude thus created was a factor in almost every case. Occasionally the cause was an affection of the ear, nose, or throat; though hardness of hearing was scarcely ever the sole reason for the trouble. In a few instances it was due to a slight fault in the vocal organs; and in others, to bad production of the voice. In no case was it due to an abnormally low register; and tine deafness was found to be non-existent. In order to remedy the defect the child was helped to locates notes, then persuaded to sing ascending scales, and also made to attempt to sing songs of very easy type. The vowel sound ‘loo’ frequently, but not exclusively used, was found to be a splendid corrective of bad voice-production. Constant encouragement was given; and great patience and determination were necessary. The good results of the work were evident in the increased interest in musical activities, and in the general enthusiasm of those who had been taught to sing

Development of single crystal beta-alumina membrane

Feasibility of crystal growth technique for beta alumina membrane from molybdenum, tungsten, and iridiu

Challenging the Discretionary Aspects of a Sentence in Pennsylvania: Commonwealth v. Mastromarino

Recent Decision

CSI sensing and control: Analytical and experimental results

Recent work on structural identification and large-angle maneuvers with vibration suppression was presented. The recent work has sought to balance structural and controls analysis activities by involving the analysts directly in the validation and experimental aspects of the research. Some new sensing, actuation, system identification, and control concepts were successfully implemented. An overview of these results is given

Protein tyrosine kinase but not protein kinase C inhibition blocks receptor induced alveolar macrophage activation

The selective enzyme inhibitors genistein and Ro 31-8220 were used to assess the importance of protein tyrosine kinase (PTK) and protein kinase C (PKC), respectively, in N-formyl-methionyl-leucyl-phenylalanine (FMLP) induced generation of superoxide anion and thromboxane B2 (TXB2) in guinea-pig alveolar macrophages (AM). Genistein (3–100 μM) dose dependently inhibited FMLP (3 nM) induced superoxide generation in non-primed AM and TXB2 release in non-primed or in lipopolysaccharide (LPS) (10 ng/ml) primed AM to a level > 80% but had litle effect up to 100 μM on phorbol myristate acetate (PMA) (10 nM) induced superoxide release. Ro 31-8220 inhibited PMA induced superoxide generation (IC50 0.21 ± 0.10 μM) but had no effect on or potentiated (at 3 and 10 μM) FMLP responses in non-primed AM. In contrast, when present during LPS priming as well as during FMLP challenge Ro 31-8220 (10 μM) inhibited primed TXB2 release by > 80%. The results indicate that PTK activation is required for the generation of these inflammatory mediators by FMLP in AM. PKC activation appears to be required for LPS priming but not for transducing the FMLP signal; rather, PKC activation may modulate the signal by a negative feedback mechanism

Clinical surveillance of thrombotic microangiopathies in Scotland, 2003-2005

The prevalence, incidence and outcomes of haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopaenic purpura (TTP) are not well established in adults or children from prospective studies. We sought to identify both outcomes and current management strategies using prospective, national surveillance of HUS and TTP, from 2003 to 2005 inclusive. We also investigated the links between these disorders and factors implicated in the aetiology of HUS and TTP including infections, chemotherapy, and immunosuppression. Most cases of HUS were caused by verocytotoxin-producing Escherichia coli (VTEC), of which serotype O157 predominated, although other serotypes were identified. The list of predisposing factors for TTP was more varied although use of immunosuppressive agents and severe sepsis, were the most frequent precipitants. The study demonstrates that while differentiating between HUS and TTP is sometimes difficult, in most cases the two syndromes have quite different predisposing factors and clinical parameters, enabling clinical and epidemiological profiling for these disorders