Pin Structures from Zirconium Dioxide Used In Various Areas of the Dental Arch

One of the ways to preserve the morphological and functional unity of the dentition is the restoration of defects in the hard tissues of the teeth with a total or subtotal loss of the crown part, since the loss of the crown part of the tooth leads to an uneven distribution of masticatory pressure, which, in turn, causes further destruction of the dentoalveolar system. With the complete absence of the crown part of the tooth, root removal is not always justified. The preservation of roots that can be used for prosthetics prevents the formation of defects, deformations of the dentition and atrophy of the jaw bone tissue (E.A. Bragin, 2001, 2003; N.I. Lesnykh, 2004). Treatment of defects in hard tissues of teeth as a result of complicated caries is an important problem in dentistry, which is due not only to the high prevalence of this pathology, but also to the complexity and laboriousness of medical manipulations, a large number of complications with poor-quality treatment. Despite new materials, technologies and instruments appearing in practice, the requirements for reliable and effective orthopedic treatment are constantly increasing. At the same time, the final stage of the treatment of complicated caries is of great importance - the restoration of the crown part of the tooth, which largely affects the outcome of the disease

Pin Structures from Zirconium Dioxide Used In Various Areas of the Dental Arch

One of the ways to preserve the morphological and functional unity of the dentition is the restoration of defects in the hard tissues of the teeth with a total or subtotal loss of the crown part, since the loss of the crown part of the tooth leads to an uneven distribution of masticatory pressure, which, in turn, causes further destruction of the dentoalveolar system. With the complete absence of the crown part of the tooth, root removal is not always justified. The preservation of roots that can be used for prosthetics prevents the formation of defects, deformations of the dentition and atrophy of the jaw bone tissue (E.A. Bragin, 2001, 2003; N.I. Lesnykh, 2004). Treatment of defects in hard tissues of teeth as a result of complicated caries is an important problem in dentistry, which is due not only to the high prevalence of this pathology, but also to the complexity and laboriousness of medical manipulations, a large number of complications with poor-quality treatment. Despite new materials, technologies and instruments appearing in practice, the requirements for reliable and effective orthopedic treatment are constantly increasing. At the same time, the final stage of the treatment of complicated caries is of great importance - the restoration of the crown part of the tooth, which largely affects the outcome of the disease

Regulation of Endocytic Recycling of KCNQ1/KCNE1 Potassium Channels.

Stress-dependent regulation of cardiac action potential duration is mediated by the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis. It is accompanied by an increased magnitude of the slow outward potassium ion current, I(Ks). KCNQ1 and KCNE1 subunits coassemble to form the I(Ks) channel. Mutations in either subunit cause long QT syndrome, an inherited cardiac arrhythmia associated with an increased risk of sudden cardiac death. Here we demonstrate that exocytosis of KCNQ1 proteins to the plasma membrane requires the small GTPase RAB11, whereas endocytosis is dependent on RAB5. We further demonstrate that RAB-dependent KCNQ1/KCNE1 exocytosis is enhanced by the serum- and glucocorticoid-inducible kinase 1, and requires phosphorylation and activation of phosphoinositide 3-phosphate 5-kinase and the generation of PI(3,5)P(2). Identification of KCNQ1/KCNE1 recycling and its modulation by serum- and glucocorticoid-inducible kinase 1-phosphoinositide 3-phosphate 5-kinase -PI(3,5)P(2) provides a mechanistic insight into stress-induced acceleration of cardiac repolarization

Regulation of endocytic recycling of KCNQ1/KCNE1 potassium channels

Stress-dependent regulation of cardiac action potential duration is mediated by the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis. It is accompanied by an increased magnitude of the slow outward potassium ion current, I(Ks). KCNQ1 and KCNE1 subunits coassemble to form the I(Ks) channel. Mutations in either subunit cause long QT syndrome, an inherited cardiac arrhythmia associated with an increased risk of sudden cardiac death. Here we demonstrate that exocytosis of KCNQ1 proteins to the plasma membrane requires the small GTPase RAB11, whereas endocytosis is dependent on RAB5. We further demonstrate that RAB-dependent KCNQ1/KCNE1 exocytosis is enhanced by the serum- and glucocorticoid-inducible kinase 1, and requires phosphorylation and activation of phosphoinositide 3-phosphate 5-kinase and the generation of PI(3,5)P(2). Identification of KCNQ1/KCNE1 recycling and its modulation by serum- and glucocorticoid-inducible kinase 1-phosphoinositide 3-phosphate 5-kinase -PI(3,5)P(2) provides a mechanistic insight into stress-induced acceleration of cardiac repolarization

Long QT Syndrome-Associated Mutations in KCNQ1 and KCNE1 Subunits Disrupt Normal Endosomal Recycling of IKs Channels.

Physical and emotional stress is accompanied by release of stress hormones such as the glucocorticoid cortisol. This hormone upregulates the serum- and glucocorticoid-inducible kinase (SGK)1, which in turn stimulates I(Ks), a slow delayed rectifier potassium current that mediates cardiac action potential repolarization. Mutations in I(Ks) channel alpha (KCNQ1, KvLQT1, Kv7.1) or beta (KCNE1, IsK, minK) subunits cause long QT syndrome (LQTS), an inherited cardiac arrhythmia associated with increased risk of sudden death. Together with the GTPases RAB5 and RAB11, SGK1 facilitates membrane recycling of KCNQ1 channels. Here, we show altered SGK1-dependent regulation of LQTS-associated mutant I(Ks) channels. Whereas some mutant KCNQ1 channels had reduced basal activity but were still activated by SGK1, currents mediated by KCNQ1(Y111C) or KCNQ1(L114P) were paradoxically reduced by SGK1. Heteromeric channels coassembled of wild-type KCNQ1 and the LQTS-associated KCNE1(D76N) mutant were similarly downregulated by SGK1 because of a disrupted RAB11-dependent recycling. Mutagenesis experiments indicate that stimulation of I(Ks) channels by SGK1 depends on residues H73, N75, D76, and P77 in KCNE1. Identification of the I(Ks) recycling pathway and its modulation by stress-stimulated SGK1 provides novel mechanistic insight into potentially fatal cardiac arrhythmias triggered by physical or psychological stress

Ubiquitin–proteasome degradation of serum- and glucocorticoid-regulated kinase-1 (SGK-1) is mediated by the chaperone-dependent E3 ligase CHIP

SGK-1 (serum- and glucocorticoid-regulated kinase-1) is a stress-induced serine/threonine kinase that is phosphorylated and activated downstream of PI3K (phosphoinositide 3-kinase). SGK-1 plays a critical role in insulin signalling, cation transport and cell survival. SGK-1 mRNA expression is transiently induced following cellular stress, and SGK-1 protein levels are tightly regulated by rapid proteasomal degradation. In the present study we report that SGK-1 forms a complex with the stress-associated E3 ligase CHIP [C-terminus of Hsc (heat-shock cognate protein) 70-interacting protein]; CHIP is required for both the ubiquitin modification and rapid proteasomal degradation of SGK-1. We also show that CHIP co-localizes with SGK-1 at or near the endoplasmic reticulum. CHIP-mediated regulation of SGK-1 steady-state levels alters SGK-1 kinase activity. These data suggest a model that integrates CHIP function with regulation of the PI3K/SGK-1 pathway in the stress response