906 research outputs found

    STUDY OF THE NUTRITION OF CHILDREN AGED 6 YEARS IN CONDITIONS OF SEMIBOARDING-SCHOOL OF EDUCATION

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    EXPERIMENTAL INVESTIGATION OF THE EFFECT OF PERORALLY APPLIED ALUMINIUM ON THE STRUCTURE AND FUNCTION OF SOME INTERNAL ORGANS. LUNG ALTERATIONS IN RATS

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    The authors examined the lung lesions caused by peroral aluminium application as a 0,1 % solution of AlƐĀ”l3 in a dose of 3 mg Al3+/kg b. w. for 40 days in a total of 126 white male rats (70 experimental and 56 control). Visible structural alterations were established on the 15th day of the trial consisting in desquamation of bronchial epithelium, enhanced pmounts of acid glucosaminoglycans in the cell cytoplasm and irregular disposition of cells. Later on, the activity of SDH, alkaline phosphatase, and ATP-ase decreased but acid phosphatase activity increased. Connective-tissue fibres grew up in the wall of some bronchi. These morphological findings suggest that although perorally accepted, AlƐĀ”l3 induced structural lesions in the lungs as well as metabolic disturbances in the bronchial mucosa which depended on the duration of treatment

    MORPHOLOGICAL ALTERATIONS IN SPLEEN AND LYMPH NODES OF EXPERIMENTAL RATS TREATED WITH AICI3

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    Rare KIT (CD117) expression in multiple myeloma abrogates the usefulness of imatinib mesylate treatment

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    Background: Imatinib mesylate blocks the tyrosine kinase activity of KIT (CD117) and is an effective treatment for gastrointestinal stromal tumors. In multiple myeloma, KIT expression has been detected by flow cytometry in about 33% of specimens, but no previous immunohistochemical assessment has yet been made of the expression pattern of KIT. Materials and methods: We performed immunohistochemical analyses of 100 patients, including 72 with multiple myeloma (MM), 8 with lymphoplasmacytic lymphoma (LPL), 10 with monoclonal gammopathy of undetermined significance (MGUS) and 10 with reactive plasmocytosis. One KIT-positive MM was sequenced using polymerase chain reaction analysis. Results: In MM, only 2 cases (2.8%) were KIT positive. The great majority of the cases (97, 2%) did not express the KIT receptor tyrosine kinase. No mutation of the c-kit gene was detected. Conclusions: KIT expression is a rare event in MM and not detectable in MGUS and LPL. Therefore, treatment with imatinib is unlikely to be effective in these patient

    STUDIES ON CYTOMEGALOVIRAL (CMV) INFECTIONS IN NEWBORN CHILDREN

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    IT for Innovative Educational Environments: Exploring, Authoring and Programming

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    The paper presents a novel approach based on using a single educational environment to achieve various methods for supporting educational activities ā€“ exploring prebuilt learning modules, using authoring tools to create educational modules and programming activities. This approach builds a solid foundation for subject-neutral and multidisciplinary applications and utilized modern IT techniques like virtual reality, interactivity and explorativity

    STUDY ON Š¢ŠŠ• DYSENTERY EPIDEMIC, CAUSED Š’Š£ BACTERIUM DYSENTERIAE SONNE WIŠ¢H CONCOMIŠ¢ANT DEVELOPMENT OF CATARRHAL INFLAMMATION OF UPPER RESPIRATORY WAYS (CURW) IN Š CLOSED CHILDREN'S COMMUNIŠ¢Y

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    Dysentery epidemics, caused bу Š’Š°Ńt. dysenteriae Sonne have been described rather oflen in the past decade, especially Š°mong children groups. More rŠ°rŠµlу Š° combined course of the dysentery epidemic is reported with epidemic caused bу adenoviral or other etiological factors. In this country, Sheljazkov and Radev, Slanishev, Nedialkova and Belova have observed clinical angina in patients with dysentery. In the literature reviewed wŠµ couldn't find evidence for simultaneous development of dysentery epidemic - SŠ¾nnŠµ and catarrhal inflammation of the upper respiratory ways (CURW). The latter combination was observed in the boarding school of the village G. nŠµŠ°Š³ VŠ°rnŠ°.The first dysentery cases occurred on 3 February, 1964 Š°nd spread rapidly, reaching the peak on 11 February; the illness was controlled on 15 February. The cases with CURW almost coincide with the dynamics just described.lnformation concerning dysentery discase Š°nd CURW show that CURW morbidity rŠ°tŠµ is higher than that of dysentery. ln part of the patieŠæts Š° combination was disclosed of the two affections. The analysis of the widespreading of the illnesses according to classes, sex Š°nd dormitories enabled us of establishing the following characteristic features:Boys and girls of the lower classes Š°Š³Šµ involved in Š° greater degree bу dysentery affections Š°nd less bу CURW. The contrary is valid for the children of the upper classes. The morbidity Š³Š°tŠµ of dysentery among girls is higher as compared to boys, whereas morbidity of CURW - higher among boys and lower among girls.The involvement of children bу dysentery Š°nd CURW according to dormitories is reverse. For instaŠæce, in II dormitory where girls live mainly of III and IV classes, the dysentery cases are 60% and CURW - 36%. whereas in IV dormitory, where boys from the VII class lived, the affected bу dysentery Š°Š³Šµ 25% and bу CURW - 75%

    Molecular interactions of ASPP1 and ASPP2 with the p53 protein family and the apoptotic promoters PUMA and Bax

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    The apoptosis stimulating p53 proteins, ASPP1 and ASPP2, are the first two common activators of the p53 protein family that selectively enable the latter to regulate specific apoptotic target genes, which facilitates yes yet unknown mechanisms for discrimination between cell cycle arrest and apoptosis. To better understand the interplay between ASPP- and p53-family of proteins we investigated the molecular interactions between them using biochemical methods and structure-based homology modelling. The data demonstrate that: (i) the binding of ASPP1 and ASPP2 to p53, p63 and p73 is direct; (ii) the C-termini of ASPP1 and ASPP2 interact with the DNA-binding domains of p53 protein family with dissociation constants, Kd, in the lower micro-molar range; (iii) the stoichiometry of binding is 1:1; (iv) the DNA-binding domains of p53 family members are sufficient for these proteinā€“protein interactions; (v) EMSA titrations revealed that while tri-complex formation between ASPPs, p53 family of proteins and PUMA/Bax is mutually exclusive, ASPP2 (but not ASPP1) formed a complex with PUMA (but not Bax) and displaced p53 and p73. The structure-based homology modelling revealed subtle differences between ASPP2 and ASPP1 and together with the experimental data provide novel mechanistic insights
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