Optimal Taxation of Banks in Financial Sector Regulation in Uzbekistan: Practical Approach

Global financial crisis made most of advanced and developing economies review and re-examine the relevanceof fiscal and banking policy regimes. Existing fiscal gap and financial market disorders led to the introduction ofnew taxes and mandatory fees for banks for double edged reasons – bridging the fiscal gap and bank capitalregulation. In a harsh economic condition most banks required the governments to rethink the taxation policy forfinancial institutions. Most policymakers and researchers are devising diverse proposals on optimal taxationwhich meet the needs of both parties. This paper studies the international bank taxation policies and recentdevelopment, and examines the opportunities of introduction of optimal taxation for banks in banking system ofUzbekistan.Keywords: taxation for banks, optimal taxation, tax position, multiple taxation method, Uzbekista

Capital Outflow and the Place of Russia in Core–Periphery Relationships

The problem of capital outflow from the Russian economy is considered in three aspects: export of capital, flight of capital and drain of capital. Permanent net capital outflow through private and public channels allows the state to devalue the ruble and create a favorable environment for export-oriented mining industries. This circumstance, firstly, inhibits the qualitative growth of the Russian economy, and secondly, is a sign of its peripheral nature in the global capitalism

Synergetic effect of recoverin and calmodulin on regulation of rhodopsin kinase.

Phosphorylation of photoactivated rhodopsin by rhodopsin kinase (RK or GRK1), a first step of the phototransduction cascade turnoff, is under the control of Ca(2+)/recoverin. Here, we demonstrate that calmodulin, a ubiquitous Ca(2+)-sensor, can inhibit RK, though less effectively than recoverin does. We have utilized the surface plasmon resonance technology to map the calmodulin binding site in the RK molecule. Calmodulin does not interact with the recoverin-binding site within amino acid residues M1-S25 of the enzyme. Instead, the high affinity calmodulin binding site is localized within a stretch of amino acid residues V150-K175 in the N-terminal regulatory region of RK. Moreover, the inhibitory effect of calmodulin and recoverin on RK activity is synergetic, which is in agreement with the existence of separate binding sites for each Ca(2+)-sensing protein. The synergetic inhibition of RK by both Ca(2+)-sensors occurs over a broader range of Ca(2+)-concentration than by recoverin alone, indicating increased Ca(2+)-sensitivity of RK regulation in the presence of both Ca(2+)-sensors. Taken together, our data suggest that RK regulation by calmodulin in photoreceptor cells could complement the well-known inhibitory effect of recoverin on RK

G protein-coupled receptor kinase 2 (GRK2) is localized to centrosomes and mediates epidermal growth factor-promoted centrosomal separation.

G protein-coupled receptor kinases (GRKs) play a central role in regulating receptor signaling, but recent studies suggest a broader role in modulating normal cellular functions. For example, GRK5 has been shown to localize to centrosomes and regulate microtubule nucleation and cell cycle progression. Here we demonstrate that GRK2 is also localized to centrosomes, although it has no role in centrosome duplication or microtubule nucleation. Of interest, knockdown of GRK2 inhibits epidermal growth factor receptor (EGFR)-mediated separation of duplicated centrosomes. This EGFR/GRK2-mediated process depends on the protein kinases mammalian STE20-like kinase 2 (Mst2) and Nek2A but does not involve polo-like kinase 1. In vitro analysis and dominant-negative approaches reveal that GRK2 directly phosphorylates and activates Mst2. Collectively these findings demonstrate that GRK2 is localized to centrosomes and plays a central role in mitogen-promoted centrosome separation most likely via its ability to phosphorylate Mst2

Resonance electron interaction with five-membered heterocyclic compounds: Vibrational Feshbach resonances and hydrogen-atom stripping

Low-energy (0–15 eV) resonance electron attachment to a series of five-membered heterocyclic rings (isoxazole, imidazole, pyrazole, pyrrole, 1-methyl-, and 2-methylimidazole) is studied under gas-phase conditions by means of electron transmission spectroscopy and dissociative electron attachment spectroscopy (DEAS). Experimental spectral features are assigned on the basis of Hartree-Fock and density functional theory calculations. Sharp features, with a width of less than 0.1 eV, observed in the electron transmission spectra of imidazole, pyrazole, and pyrrole close to 0.45 eV, i.e., well below the energy of their lowest-lying π∗ shape resonances detected at 1.90, 1.87, and 2.33 eV, respectively, are associated with formation of negative ion states bound by long-range electron-molecule interactions. Effective range theory calculations which include both dipolar and polarization interactions support this interpretation. In addition to the general observation of cleavage of the N–H bond at incident electron energies close to 2 eV, elimination of as many as three hydrogen atoms from the molecular negative ions is detected at higher energies by DEAS with the only exception of methylated imidazoles. This complex process is associated with ring opening and formation of diatomic hydrogen as one of the neutral fragments, as indicated by the calculations to satisfy the energetic requirements. The present results are of importance for understanding the basic mechanisms of damages caused in living tissues by high-energy radiations

Structural and Functional Analysis of a β2-Adrenergic Receptor Complex with GRK5.

The phosphorylation of agonist-occupied G-protein-coupled receptors (GPCRs) by GPCR kinases (GRKs) functions to turn off G-protein signaling and turn on arrestin-mediated signaling. While a structural understanding of GPCR/G-protein and GPCR/arrestin complexes has emerged in recent years, the molecular architecture of a GPCR/GRK complex remains poorly defined. We used a comprehensive integrated approach of cross-linking, hydrogen-deuterium exchange mass spectrometry (MS), electron microscopy, mutagenesis, molecular dynamics simulations, and computational docking to analyze GRK5 interaction with the β2-adrenergic receptor (β2AR). These studies revealed a dynamic mechanism of complex formation that involves large conformational changes in the GRK5 RH/catalytic domain interface upon receptor binding. These changes facilitate contacts between intracellular loops 2 and 3 and the C terminus of the β2AR with the GRK5 RH bundle subdomain, membrane-binding surface, and kinase catalytic cleft, respectively. These studies significantly contribute to our understanding of the mechanism by which GRKs regulate the function of activated GPCRs. PAPERCLIP

Computational Strategy for Graphene: Insight from Odd Electrons Correlation

The correlation of odd electrons in graphene turns out to be significant so that the species should be attributed to correlated ones. This finding profoundly influences the computational strategy addressing it to multireference computational schemes. Owing to serious problems related to the schemes realization, a compromise can be suggested by using single-determinant approaches based on either Hartree-Fock or Density-Functional theory in the form of unrestricted open-shell presentation. Both computational schemes enable to fix the electron correlation, while only the Hartree-Fock theory suggests a set of quantities to be calculated that can quantitatively characterize the electron correlation and be used for a quantitative description of such graphene properties as magnetism, chemical reactivity, and mechanical response. The paper presents concepts and algorithms of the unrestricted Hartree-Fock theory applied for the consideration of magnetic properties of nanographenes, their chemical modification by the example of stepwise hydrogenation, as well as a possible governing the electron correlation by the carbon skeleton deformation.Comment: 17 pages, 11 figures, 3 table

FAN1 Removes Triplet Repeat Extrusions via a PCNA- And RFC-Dependent Mechanism

Human genome-wide association studies have identified FAN1 and several DNA mismatch repair (MMR) genes as modifiers of Huntington’s disease age of onset. In animal models, FAN1 prevents somatic expansion of CAG triplet repeats, whereas MMR proteins promote this process. To understand the molecular basis of these opposing effects, we evaluated FAN1 nuclease function on DNA extrahelical extrusions that represent key intermediates in triplet repeat expansion. Here, we describe a strand-directed, extrusion-provoked nuclease function of FAN1 that is activated by RFC, PCNA, and ATP at physiological ionic strength. Activation of FAN1 in this manner results in DNA cleavage in the vicinity of triplet repeat extrahelical extrusions thereby leading to their removal in human cell extracts. The role of PCNA and RFC is to confer strand directionality to the FAN1 nuclease, and this reaction requires a physical interaction between PCNA and FAN1. Using cell extracts, we show that FAN1-dependent CAG extrusion removal relies on a very short patch excision-repair mechanism that competes with MutSβ-dependent MMR which is characterized by longer excision tracts. These results provide a mechanistic basis for the role of FAN1 in preventing repeat expansion and could explain the antagonistic effects of MMR and FAN1 in disease onset/progression

Особенности МРТ-семиотики височно-нижнечелюстного сустава у пациентов с дистальной окклюзией зубных рядов при разных клинических вариантах течения дисфункции височно-нижнечелюстного сустава

Aim: to study stigmatization of connective tissue dysplasia and androgenic profiles as potential markers associated with temporomandibular joint disorders, compared with magnetic resonance tomography imaging of the temporomandibular joint in patients with different clinical variants of its dysfunction. Materials and methods. 40 patients with distal occlusion 35 women (87.5%) and 5 men (12.5%) and dysfunction of the temporomandibular joint (from mild to severe). The clinical examination included: evaluation of connective tissue dysplastic stigmatization; Magnetic resonance tomography on Vantage Atlas-X 1.5 T, hormones concentrations estimation by Enzyme immunoassay: testosterone-estradiol binding globulin, total and free testosterone, estradiol, free androgen index. All patients were devided into two groups according to the Scale of severness of temporomandibular “joint dysfunction syndrome”: the 1-st mild group (0-6 score) included 18 patients (45,0%) with less than 3 displastic stigmatization; the 2nd severe group (1012 scores) - 22 patients with 6 and more dysplastic stigmatization. Results. In the first group of mildly symptomatic patients without complaints in 56.6% cases a combination of up to 2, in 44.4% - up to three clinical manifestations, the temporomandibular joint dysfunction was found. Signs of intra violations in each fourth case reflected changes, characteristic of early stages of osteoarthritis. The combination frequency of over 3 clinical manifestations in patients of the second group (100%), combined with magnetic resonance imaging of soft tissue and bone changes in intra-changes with the hallmark of chronic synovitis - the presence of a pathological effusion in 45.5% of cases. The detected significant increase in androgens in patients of the second group correlated with the severity of the studied disease and the degree of morphological changes. Conclusion. The extent of anatomical and functional changes in the joint correlates with increasing frequency of detection, bilateral localization and involvement into the process of other joint elements (bone, soft tissue, muscular system), as well as phenotypic burdened stigma DST and hyperandrogenism in patients with distal occlusion.Цель исследования: изучение в качестве потенциальных маркеров, ассоциированных с повреждением височно-нижнечелюстного сустава (ВНЧС), стигматизации по дисплазии соединительной ткани (ДСТ), андрогенного профиля в сопоставлении с МР-томографической картиной ВНЧС у пациентов с разными клиническими вариантами его дисфункции. Материал и методы. Проанализированы результаты обследования 40 пациентов с дистальной окклюзией зубных рядов (35 (87,5%) женщин и 5 (12,5%) мужчин) и дисфункцией ВНЧС (легкой и тяжелой степени). Объем обследования пациентов: клиническое обследование с оценкой стигматизации ДСТ; МРТ на аппарате Vantage Atlas-X 1,5 T; определение концентраций гормонов методом иммуноферментного анализа (тестостерон-эстрадиол, связывающий глобулин, общий и свободный тестостерон, эстрадиол, расчет индекса свободных андрогенов). На основании “Шкалы для определения индекса тяжести синдрома ВНЧС пациенты были распределены на 2 группы: в 1-ю группу легкой степени (0-6 баллов) тяжести включены 18 (45,0%) пациентов с наличием не более 3 стигм ДСТ, во 2-ю - тяжелой степени (10-12 баллов) - 22 (55,0%) пациента с 6 и более фенотипическими стигмами ДСТ Результаты. У пациентов “малосимптомной” 1-й группы при отсутствии жалоб сочетания до 2 клинических проявлений дисфункции ВНЧС выявлены в 56,6%, до 3 - в 44,4%. Признаки внутрисуставных нарушений в каждом 4-м случае отражали изменения, характерные для начальных стадий остеоартроза. Частота сочетания более 3 клинических проявлений у пациентов 2-й группы (100%) сочеталась с более выраженными на МР-томограммах изменениями мягкотканных и костных внутрисуставных изменений с отличительным признаком хронического синовита - наличие патологического выпота в 45,5% случаев. Обнаруженные достоверные повышения уровней андрогенов у пациентов 2-й группы соотносились с тяжестью изучаемой патологии и выраженностью морфологических изменений. Заключение. Степень анатомо-функциональных изменений в суставе коррелирует с возрастающей частотой их выявления, двусторонней локализацией и вовлечением в процесс большего количества элементов сустава (костных, мягкотканных, мышечного аппарата), а также отягощенностью фенотипическими стигмами ДСТ и гиперандрогенией у пациенток с дистальной окклюзией