Preschool Children’s Speech Pedagogical Sound Culture Correction

Objective: The article aims to reveal the features of correction of the sound culture of the preschool-age children's speech, the effectiveness of which has been tested experimentally. Background: The sound culture of speech is a multicomponent formation, which covers the phonetic correctness of speech; general language skills and orthoepic correctness of speech. Pedagogical correction of the sound culture of speech is focused on the correct the errors caused by a violation of the sound articulation, sound pronunciation, orthoepic norms of pronunciation, voice strength, etc. Method: In the study, the author's method of pedagogical correction of the sound culture of children’s speech was used. Also, it was used comparative analysis and method of successive analysis of adjustment variants of the speech sound culture. Results: An individual model of pedagogical correction of the sound culture of the child's speech was developed. Training to deepen knowledge, improvement of abilities, and skills of teachers were held. The exercises in sound pronunciation and intonational speech expressiveness were developed. Conclusion: Positive dynamics of developmental levels of the sound culture of children’s speech, which has been confirmed by the results of quantitative and qualitative analysis, confirms the effectiveness of the experimental methods of pedagogical correction of the sound culture of speech

Evidence of a kallikrein inhibitor in human kidney. A new ring of the kallikrein-renin-angiotensin-aldosterone chain

By means of immunohistochemical reactions, the authors proved the inhibitor II-related immunoreactivity in distal convoluted tubules of human kidney. A sharp inhibitor II-related immunoreactivity was also present in the blood vessels' wall. On the contrary, in the wall of proximal tubules and glomeruli only low reactivity was found. The demonstration of an inhibitor II-related immunoreactivity in the distal convoluted tubules and vessels of human kidney represents a strong evidence that an inhibitor of kallikrein exists and acts also in humans as an important key in the kallikrein-renin-angiotensin aldosterone chain and hitherto confirms the experimental data of the literature. The proved inhibitor in the human kidney may intervene in the modulation of the kallikrein-kinin system and thus represents a key role in the intrarenal mechanisms related to the blood flow and arterial pressure regulation

Venous wall ultrastructure in generalized venomegaly.

The ultrastructure of thè v. colica sinistra in a case of generalized vasomegaìy in man was examined. Elastic material was found in three forms: as a lightly osmiophii amorphous material bordering on myocytes, as a highly osmiophii elastic membrana, and as highly osmiophii slim elastic fibres of different orientation in thè tunica media and adventitia. The slightly osmiophii elastic material is assumed to be newly formed. by pinocytotic activity of thè myocytes. The highly osmiophii elastic material indicatss its impairment. No typical atherosclerotic changes were found in thè examined vein. Based on a comparison with previous findings in thè case of vasomegaìy of thè a. mesenterica inferior, thè authors conclude that thè venomegaly phenomenon is connected with degenerative changes in thè elastic material of thè vessel wall

Cmr1/WDR76 defines a nuclear genotoxic stress body linking genome integrity and protein quality control

DNA replication stress is a source of genomic instability. Here we identify ​changed mutation rate 1 (​Cmr1) as a factor involved in the response to DNA replication stress in Saccharomyces cerevisiae and show that ​Cmr1—together with ​Mrc1/​Claspin, ​Pph3, the chaperonin containing ​TCP1 (CCT) and 25 other proteins—define a novel intranuclear quality control compartment (INQ) that sequesters misfolded, ubiquitylated and sumoylated proteins in response to genotoxic stress. The diversity of proteins that localize to INQ indicates that other biological processes such as cell cycle progression, chromatin and mitotic spindle organization may also be regulated through INQ. Similar to ​Cmr1, its human orthologue ​WDR76 responds to proteasome inhibition and DNA damage by relocalizing to nuclear foci and physically associating with CCT, suggesting an evolutionarily conserved biological function. We propose that ​Cmr1/​WDR76 plays a role in the recovery from genotoxic stress through regulation of the turnover of sumoylated and phosphorylated proteins

The prion-like RNA-processing protein HNRPDL forms inherently toxic amyloid-like inclusion bodies in bacteria

BACKGROUND: The formation of protein inclusions is connected to the onset of many human diseases. Human RNA binding proteins containing intrinsically disordered regions with an amino acid composition resembling those of yeast prion domains, like TDP-43 or FUS, are being found to aggregate in different neurodegenerative disorders. The structure of the intracellular inclusions formed by these proteins is still unclear and whether these deposits have an amyloid nature or not is a matter of debate. Recently, the aggregation of TDP-43 has been modelled in bacteria, showing that TDP-43 inclusion bodies (IBs) are amorphous but intrinsically neurotoxic. This observation raises the question of whether it is indeed the lack of an ordered structure in these human prion-like protein aggregates the underlying cause of their toxicity in different pathological states. RESULTS: Here we characterize the IBs formed by the human prion-like RNA-processing protein HNRPDL. HNRPDL is linked to the development of limb-girdle muscular dystrophy 1G and shares domain architecture with TDP-43. We show that HNRPDL IBs display characteristic amyloid hallmarks, since these aggregates bind to amyloid dyes in vitro and inside the cell, they are enriched in intermolecular β-sheet conformation and contain inner amyloid-like fibrillar structure. In addition, despite their ordered structure, HNRPDL IBs are highly neurotoxic. CONCLUSIONS: Our results suggest that at least some of the disorders caused by the aggregation of human prion-like proteins would rely on the formation of classical amyloid assemblies rather than being caused by amorphous aggregates. They also illustrate the power of microbial cell factories to model amyloid aggregation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12934-015-0284-7) contains supplementary material, which is available to authorized users