Sulfate Removal from Reject Brined in Inland Desalination with Zero Liquid Discharge

Sulfate is one of the most problematic ions present in reject brine in desalination systems due to its high potential of scale formation and membrane fouling; making it an obstacle in the application of zero liquid discharge. The ultra-high lime with aluminum process (UHLA) has shown to effectively remove sulfate. This research involves the study of sulfate removal from the nano-filtration unit in the zero liquid discharge system for inland desalination via a two-stage process using a calcium source to remove sulfate in the first stage and implementing the UHLA process in the second stage. The kinetics, equilibrium characteristics, and effects of different parameters on sulfate removal were studied. Kinetics of sulfate removal was studied on both stages of the process. The observation of fast kinetics in both stages indicated that removal kinetics is not a limitation for the application of the process. Equilibrium characteristics of the UHLA process were performed which revealed efficient sulfate removal at practical ranges of lime and aluminum doses. The effect of pH on sulfate removal in the process was studied. Results showed that sulfate removal in Stage 1 was independent of the pH of the solution while effective sulfate removal in Stage 2 was found to be above a pH of 11. The effect of initial sulfate concentrations on sulfate removal in Stage 1 was investigated and sulfate removal was mainly controlled by calcium sulfate solubility. The effect of initial chloride concentrations on sulfate removal in Stage 2 was evaluated and the results indicated that chloride has negligible effect on the removal of sulfate. Experiments concerning the effect of the recycle of calcium sulfate solids in Stage 1 showed an increase of the reaction rate. In contrast, the recycle of Stage 2 dry solids into Stage 2 revealed no effect on sulfate removal. An equilibrium model was developed to explain the equilibrium characteristics of Stage 2. It was found that a valid explanation for the chemistry of sulfate removal in Stage 2 was the formation of a solid solution consisting of ettringite and monosulfate. XRD analysis confirmed the formation of these solids

Pharmacological targeting of AKAP-directed compartmentalized cAMP signalling

The second messenger cyclic adenosine monophosphate (cAMP) can bind and activate protein kinase A (PKA). The cAMP/PKA system is ubiquitous and involved in a wide array of biological processes and therefore requires tight spatial and temporal regulation. Important components of the safeguard system are the A-kinase anchoring proteins (AKAPs), a heterogeneous family of scaffolding proteins defined by its ability to directly bind PKA. AKAPs tether PKA to specific subcellular compartments, and they bind further interaction partners to create local signalling hubs. The recent discovery of new AKAPs and advances in the field that shed light on the relevance of these hubs for human disease highlight unique opportunities for pharmacological modulation. This review exemplifies how interference with signalling, particularly cAMP signalling, at such hubs can reshape signalling responses and discusses how this could lead to novel pharmacological concepts for the treatment of disease with an unmet medical need such as cardiovascular disease and cancer

The A-kinase anchoring protein (AKAP) glycogen synthase kinase 3β interaction protein (GSKIP) regulates β-catenin through its interactions with both protein kinase A (PKA) and GSK3β

The A-kinase anchoring protein (AKAP) GSK3beta interaction protein (GSKIP) is a cytosolic scaffolding protein binding protein kinase A (PKA) and glycogen synthase kinase 3beta (GSK3beta). Here we show that both the AKAP function of GSKIP, i.e. its direct interaction with PKA, and its direct interaction with GSK3beta are required for the regulation of beta-catenin and thus Wnt signaling. A cytoplasmic destruction complex targets beta-catenin for degradation and thus prevents Wnt signaling. Wnt signals cause beta-catenin accumulation and translocation into the nucleus, where it induces Wnt target gene expression. GSKIP facilitates control of the beta-catenin stabilizing phosphorylation at Ser-675 by PKA. Its interaction with GSK3beta facilitates control of the destabilizing phosphorylation of beta-catenin at Ser-33/Ser-37/Thr-41. The influence of GSKIP on beta-catenin is explained by its scavenger function; it recruits the kinases away from the destruction complex without forming a complex with beta-catenin. The regulation of beta-catenin by GSKIP is specific for this AKAP as AKAP220, which also binds PKA and GSK3beta, did not affect Wnt signaling. We find that the binding domain of AKAP220 for GSK3beta is a conserved GSK3beta interaction domain (GID), which is also present in GSKIP. Our findings highlight an essential compartmentalization of both PKA and GSK3beta by GSKIP, and ascribe a function to a cytosolic AKAP-PKA interaction as a regulatory factor in the control of canonical Wnt signaling. Wnt signaling controls different biological processes, including embryonic development, cell cycle progression, glycogen metabolism, and immune regulation; deregulation is associated with diseases such as cancer, type 2 diabetes, inflammatory, and Alzheimer's and Parkinson's diseases

The microstructure and hardness of casting a solid brake disc after late graphitizing modification

The features of graphite formation in hypoeutectic and hypereutectic gray cast iron are considered. It is shown that this process in hypoeutectic gray cast irons is easier to control than in hypereutectic, because the formation of a predominantly rectilinear uniformly distributed graphite with a smaller size range and the presence of other distributions is achieved by an one-stage operation of ladle graphitization. The structure of graphite in hypereutectic gray cast irons is characterized by a large variety of its shapes, sizes and distributions, and it is also less technologically stable and controllable. Its characteristics can be approximated to the structure of hypoeutectic gray cast iron due to the obligatory second stage of graphitization. The microstructure and hardness of casting a solid brake disc after late graphitizing modification in a mold are investigated. The content of interdendritic distributions of graphite PGr8, PGr9 and short inclusions of graphite PGd45-90 (GOST 3443-87) was minimized due to the operation of the secondary (late) graphitizing modification. And Brinell hardness of the solid brake disc meets production requirements. © Published under licence by IOP Publishing Ltd.This work is carried out within a framework of the government order (No. FZRU-2020-0011) of the Ministry of Science and Higher Education of the Russian Federation

Citron kinase controls abscission through RhoA and Anillin.

The small GTPase RhoA plays a crucial role in the different stages of cytokinesis, including contractile ring formation, cleavage furrow ingression, and midbody abscission. Citron kinase (CIT-K), a protein required for cytokinesis and conserved from insects to mammals, is currently considered a cytokinesis-specific effector of active RhoA. In agreement with previous observations, we show here that, as in Drosophila cells, CIT-K is specifically required for abscission in mammalian cells. However, in contrast with the current view, we provide evidence that CIT-K is an upstream regulator rather than a downstream effector of RhoA during late cytokinesis. In addition, we show that CIT-K is capable of physically and functionally interacting with the actin-binding protein anillin. Active RhoA and anillin are displaced from the midbody in CIT-K-depleted cells, while only anillin, but not CIT-K, is affected if RhoA is inactivated in late cytokinesis. The overexpression of CIT-K and of anillin leads to abscission delay. However, the delay produced by CIT-K overexpression can be reversed by RhoA inactivation, while the delay produced by anillin overexpression is RhoA-independent. Altogether, these results indicate that CIT-K is a crucial abscission regulator that may promote midbody stability through active RhoA and anillin

ДОМЕДИЧНА ДОПОМОГА ЯК БАЗОВА СКЛАДОВА У ФОРМУВАННІ КОМПЕТЕНТНОСТЕЙ ФАХІВЦІВ З ФІЗИЧНОЇ ТЕРАПІЇ ТА ЕРГОТЕРАПІЇ

The aim of the work – analysis of higher education standard in discipline 227 of Physical Therapy, Ergotherapy, specialty 22 of Public Health and curriculum on Physical Therapy and Ergotherapy in the aspect of competence formation on providing premedical first aid. The main body. Main stages of competence formation for providing premedical first aid in emergency situations via simulation Training in Ergotherapists students are determined. Advantages of simulation training method in medicine are listed. It is shown that equality of teacher and students helps to find out mistakes during practical skills training. It was found out that better mastering of skills is in case when results of primary and secondary examinations of victims differs according to the data of situational tasks. It is proven that feedback between a teacher and students is one of key points that will ensure better assimilation of practical skills and action algorithms by students. Conclusions. It was found out that simulation training improves formation of ergotherapists students’ competence. Additionally, this helps to arise students’ interest to subject learning. Simulation training allows students to learn algorithms of premedical first aid providing in conditions that are close to real. Obtaining of skills in critical bleeding stop, victim transfer to stable lateral position and cardiopulmonary resuscitation by ergotherapists students’ allow to provide necessary premedical assistance in cases of emergencies.Мета роботи – аналіз стандарту вищої освіти за спеціальністю 227 “Фізична терапія, ерготерапія” галузі знань 22 “Охорона здоров’я” та навчальної програми з фізичної терапії та ерготерапії в аспекті формування компетентності з надання домедичної допомоги. Основна частина. Визначено основні етапи формування компетенції для надання медичної допомоги у надзвичайних ситуаціях шляхом моделювання тренінгів у студентів-ерготерапевтів. Перераховані переваги симуляції методу навчання в медицині. Показано, що врівноваження ролей учителя та студентів допомагає виявити помилки під час тренінгу з практичних навичок. З’ясовано, що краще освоєння навичок відбувається у випадку, коли результати при первинному і вторинному огляді потерпілих відрізняються відповідно до даних ситуаційних завдань. Доведено, що зворотний зв’язок між вчителем та студентами є одним із ключових моментів, який забезпечить кращу асиміляцію алгоритмів практичних навичок і дій студентами. Висновки. Виявлено, що симуляційне навчання покращує формування компетенції студентів-ерготерапевтів. Крім того, це сприяє підвищенню інтересу студентів до вивчення предмета. Симуляційна підготовка дозволяє студентам вивчати алгоритми надання медичної допомоги в умовах, що близькі до реальності. Отримання навичок зупинки критичної кровотечі, переведення потерпілого в стабільне бокове положення та серцево-легенева реанімація дозволяють студентам-ерготерапевтам надати необхідну домедичну допомогу у разі виникнення надзвичайних ситуацій

Methodology of Natsal-COVID Wave 1: a large, quasi-representative survey with qualitative follow-up measuring the impact of COVID-19 on sexual and reproductive health in Britain [version 1; peer review: awaiting peer review]

Background: Britain’s National Surveys of Sexual Attitudes and Lifestyles (Natsal) have been undertaken decennially since 1990 and provide a key data source underpinning sexual and reproductive health (SRH) policy. The COVID-19 pandemic disrupted many aspects of sexual lifestyles, triggering an urgent need for population-level data on sexual behaviour, relationships, and service use at a time when gold-standard in-person, household-based surveys with probability sampling were not feasible. We designed the Natsal-COVID study to understand the impact of COVID-19 on the nation’s SRH and assessed the sample representativeness. Methods: Natsal-COVID Wave 1 data collection was conducted four months (29/7-10/8/2020) after the announcement of Britain’s first national lockdown (23/03/2020). This was an online web-panel survey administered by survey research company, Ipsos MORI. Eligible participants were resident in Britain, aged 18-59 years, and the sample included a boost of those aged 18-29. Questions covered participants’ sexual behaviour, relationships, and SRH service use. Quotas and weighting were used to achieve a quasi-representative sample of the British general population. Participants meeting criteria of interest and agreeing to recontact were selected for qualitative follow-up interviews. Comparisons were made with contemporaneous national probability surveys and Natsal-3 (2010-12) to understand bias. Results: 6,654 participants completed the survey and 45 completed follow-up interviews. The weighted Natsal-COVID sample was similar to the general population in terms of gender, age, ethnicity, rurality, and, among sexually-active participants, numbers of sexual partners in the past year. However, the sample was more educated, contained more sexually-inexperienced people, and included more people in poorer health. Conclusions: Natsal-COVID Wave 1 rapidly collected quasi-representative population data to enable evaluation of the early population-level impact of COVID-19 and lockdown measures on SRH in Britain and inform policy. Although sampling was less representative than the decennial Natsals, Natsal-COVID will complement national surveillance data and Natsal-4 (planned for 2022)

Cyclin-dependent kinase 18 controls trafficking of aquaporin-2 and its abundance through ubiquitin ligase STUB1, which functions as an AKAP

Arginine-vasopressin (AVP) facilitates water reabsorption in renal collecting duct principal cells through regulation of the water channel aquaporin-2 (AQP2). The hormone binds to vasopressin V2 receptors (V2R) on the surface of the cells and stimulates cAMP synthesis. The cAMP activates protein kinase A (PKA), which initiates signaling that causes an accumulation of AQP2 in the plasma membrane of the cells facilitating water reabsorption from primary urine and fine-tuning of body water homeostasis. AVP-mediated PKA activation also causes an increase in the AQP2 protein abundance through a mechanism that involves dephosphorylation of AQP2 at serine 261 and a decrease in its poly-ubiquitination. However, the signaling downstream of PKA that controls the localization and abundance of AQP2 is incompletely understood. We carried out an siRNA screen targeting 719 kinase-related genes, representing the majority of the kinases of the human genome and analyzed the effect of the knockdown on AQP2 by high-content imaging and biochemical approaches. The screening identified 13 hits whose knockdown inhibited the AQP2 accumulation in the plasma membrane. Amongst the candidates was the so far hardly characterized cyclin-dependent kinase 18 (CDK18). Our further analysis revealed a hitherto unrecognized signalosome comprising CDK18, an E3 ubiquitin ligase, STUB1 (CHIP), PKA and AQP2 that controls the localization and abundance of AQP2. CDK18 controls AQP2 through phosphorylation at serine 261 and STUB1-mediated ubiquitination. STUB1 functions as an A-kinase anchoring protein (AKAP) tethering PKA to the protein complex and bridging AQP2 and CDK18. The modulation of the protein complex may lead to novel concepts for the treatment of disorders which are caused or are associated with dysregulated AQP2 and for which a satisfactory treatment is not available, e.g., hyponatremia, liver cirrhosis, diabetes insipidus, ADPKD or heart failure

Th17-Related Genes and Celiac Disease Susceptibility

Th17 cells are known to be involved in several autoimmune or inflammatory diseases. In celiac disease (CD), recent studies suggest an implication of those cells in disease pathogenesis. We aimed at studying the role of genes relevant for the Th17 immune response in CD susceptibility. A total of 101 single nucleotide polymorphisms (SNPs), mainly selected to cover most of the variability present in 16 Th17-related genes (IL23R, RORC, IL6R, IL17A, IL17F, CCR6, IL6, JAK2, TNFSF15, IL23A, IL22, STAT3, TBX21, SOCS3, IL12RB1 and IL17RA), were genotyped in 735 CD patients and 549 ethnically matched healthy controls. Case-control comparisons for each SNP and for the haplotypes resulting from the SNPs studied in each gene were performed using chi-square tests. Gene-gene interactions were also evaluated following different methodological approaches. No significant results emerged after performing the appropriate statistical corrections. Our results seem to discard a relevant role of Th17 cells on CD risk