Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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Tytuł oryginału: Lung function and surface electromyography of intercostal muscles in cement mill workers.
Autorzy: Meo Sultan A., Azeem Muhammad A., Ghori Moinuddin G., Subhan Mirza M. F.
Źródło: Int. J. Occup. Med. Environ. Health 2002: 15 (3) s.279-287, tab., bibliogr. 48 poz.
Sygnatura GBL: 306,313

Hasła klasyfikacyjne GBL:
  • medycyna pracy
  • pulmonologia
  • toksykologia

    Typ dokumentu:
  • praca epidemiologiczna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • dorośli 19-44 r.ż.
  • dorośli 45-64 r.ż.
  • płeć męska

    Streszczenie angielskie: Impairment of pulmonary function in cement mill workers has been previously reported without considering a variety of parameters that can help evaluate more thoroughly the effect of cement dust on the respiratory system. In addition, an integrated approach has not been considered to assert the involvement of respiratory muscles. Therefore, in the present study spirometry and surface electromyography (SEMG) of intercostal muscles were used for indicating pulmonary impairment. In this study, a group of 50, apparently healthy volunteers, male cement mill workers aged 20-60 years with exposure of 13 years on average, were randomly selected. They were matched with another group of 50 control healthy male subjects in terms of age, height, weight and socioeconomic status. Both groups met the standard exclusion criteria. Spirometry was performed on an electronic spirometer, while SEMG of intercostal muscles was performed by using a chart recorder. The results demonstrated statistically significant reduction in lung function parameters i.e., force vital capacity (FVC) (p 0.0005); force expiratory volume in first second (FEV1) (p 0.0005); peak expiratory flow (PEF) (p 0.005); and maximum voluntary ventilation (MVV) (p 0.0005) in cement mill workers, when compared with controls. However, the FEV1/FVC ratio was significantly higher (p 0.025) in cement mill workers. Similarly, the parameters obtained from SEMG of intercostal muscles, i.e. number of peaks (NPO) (p 0.0005); maximum peak amplitude (MPA) (p 0.0005); peak to peak amplitude (PPA) (p 0.0005)...

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    Tytuł oryginału: Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome).
    Autorzy: Tristani-Firouzi Martin, Jensen Judy L., Donaldson Matthew R., Sansone Valeria, Meola Giovanni, Hahn Angelika, Bendahhou Said, Kwieciński Hubert, Fidziańska Anna, Plaster Nikki, Fu Ying-Hui, Ptacek Louis J., Tawil Rabi
    Źródło: J. Clin. Invest. 2002: 110 (3) s.381-388, il., tab., bibliogr. 38 poz.
    Sygnatura GBL: 310,487

    Hasła klasyfikacyjne GBL:
  • pediatria
  • genetyka
  • kardiologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • noworodki
  • niemowlęta
  • dzieci 2-5 r.ż.
  • dzieci 6-12 r.ż.
  • dzieci 13-18 r.ż.
  • dorośli 19-44 r.ż.

    Streszczenie angielskie: Andersen syndrome (AS) is a rare, inherited disorder characterized by periodic paralysis, long QT (LQT) with ventricular arrhythmias, and skeletal developmental abnormalitise. We recently established that AS is caused by mutations in KCNJ2, which encodes the inward rectifier K+ channel Kir2.1. In this report, we characterized the functional consequences of three novel and seven previously described KCNJ2 mutations using a two-microelectrode voltage-clamp technique and correlated the findings with the clinical phenotype. All mutations resulted in loss of function and dominant-negative suppression of Kir2.1 channel function. In mutation carriers, the frequency of periodick paralysis was 64 p.c. and dysmorphic features 78 p.c. LQT was the primary cardiac manifestation, present in 71 p.c. of KCNJ2 mutation carriers, with ventricular arrhythmias present in 64 p.c. While arrhythmias were common, none of our subjects suffered sudden cardiac death. To gain insight into the mechanismof arrhythmia susceptibility, we simulated the effect of reducdd Kir2.1 using a ventricular myocyte model. A reduction in Kir2.1 prolonged the termkinal phase of the cardiac action potential, and n the setting of reduced extracellular K+, nduced Na+/Ca2+ exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias. These findings suggest that the substrate for arrhythmia susceptibility in AS is distinct from the other forms of inherited LQT syndrome.

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