Emission Minimization of a Two-Stage Sour Water Stripping Unit Using Surrogate Models for Improving Heat Duty Control

Sour water are aqueous waste streams from oil refining operations, heavily contaminated with hydrogen sulfide and ammonia, which need to be stripped before reuse or disposal, avoiding damages to process and environment. Two-stage sour water stripper units are the most common technology to treat sour water for hydrogen sulfide and ammonia separation to produce reusable water and send these species respectively to Claus and ammonia plants. The first stage of a two-stage sour water unit is responsible for properly splitting hydrogen sulfide and ammonia. This work uses surrogate models to predict the limiting point of hydrogen sulfide separation in the first stage of a sour water unit, allowing more efficient heat duty control strategies to achieve the difficult split of hydrogen sulfide and ammonia and simultaneously lowering heat consumption. Failure of compliance to this limit results in unspecified stripped gas from the first stage, impeding it to directed to Claus plant, entailing loss of sulfur production and higher load of pollutant emissions from flared gases. Therefore, a precise surrogate predictor was developed to dynamically define a quasi-optimum set-point to the controller of the first stage reboiler duty based on dynamic disturbances – the first stage input factors to the surrogate model, such as hydrogen sulfide and ammonia contents of the sour water. The new control policy outperformed the traditional first stage ratio control in terms of stripped gas composition and plant stability

Coral Disease and Health Workshop: Coral Histopathology II

The health and continued existence of coral reef ecosystems are threatened by an increasing array of environmental and anthropogenic impacts. Coral disease is one of the prominent causes of increased mortality among reefs globally, particularly in the Caribbean. Although over 40 different coral diseases and syndromes have been reported worldwide, only a few etiological agents have been confirmed; most pathogens remain unknown and the dynamics of disease transmission, pathogenicity and mortality are not understood. Causal relationships have been documented for only a few of the coral diseases, while new syndromes continue to emerge. Extensive field observations by coral biologists have provided substantial documentation of a plethora of new pathologies, but our understanding, however, has been limited to descriptions of gross lesions with names reflecting these observations (e.g., black band, white band, dark spot). To determine etiology, we must equip coral diseases scientists with basic biomedical knowledge and specialized training in areas such as histology, cell biology and pathology. Only through combining descriptive science with mechanistic science and employing the synthesis epizootiology provides will we be able to gain insight into causation and become equipped to handle the pending crisis. One of the critical challenges faced by coral disease researchers is to establish a framework to systematically study coral pathologies drawing from the field of diagnostic medicine and pathology and using generally accepted nomenclature. This process began in April 2004, with a workshop titled Coral Disease and Health Workshop: Developing Diagnostic Criteria co-convened by the Coral Disease and Health Consortium (CDHC), a working group organized under the auspices of the U.S. Coral Reef Task Force, and the International Registry for Coral Pathology (IRCP). The workshop was hosted by the U.S. Geological Survey, National Wildlife Health Center (NWHC) in Madison, Wisconsin and was focused on gross morphology and disease signs observed in the field. A resounding recommendation from the histopathologists participating in the workshop was the urgent need to develop diagnostic criteria that are suitable to move from gross observations to morphological diagnoses based on evaluation of microscopic anatomy. (PDF contains 92 pages

An atlas of reproductive development in rockfishes, genus Sebastes

The genus Sebastes consists of over 100 fish species, all of which are viviparous and long-lived. Previous studies have presented schemes on the reproductive biology of a single targeted species of the genus Sebastes, but all appear to possess a similar reproductive biology as evidenced by this and other studies. This atlas stages major events during spermatogenesis, oogenesis, and embryogenesis, including atresia, in six species of Sebastes (S. alutus, S. elongatus, S. helvomaculatus, S. polyspinis, S. proriger, and S. zacentrus). Our study suggests that the male reproductive cycle of Sebastes is characterized by 11 phases of testicular development, with 10 stages of sperm development and 1 stage of spermatozoa atresia. Ovarian development was divided into 12 phases, with 10 stages of oocyte development, 1 stage of embryonic development, and 1 stage of oocyte atresia. Embryonic development up to parturition was divided into 33 stages following the research of Yamada and Kusakari (1991). Reproductive development of all six species examined followed the developmental classifications listed above which may apply to all species of Sebastes regardless of the number of broods produced annually. Multiple brooders vary in that not all ova are fertilized and progress to embryos; a proportion of ova are arrested at the pre-vitellogenic stage. Reproductive stage examples shown in this atlas use S. elongates for spermatic development, S. proriger for oocyte development, and S. alutus for embryological development, because opportunistic sampling only permitted complete analysis of each respective developmental phase for those species. The results of this study and the proposed reproductive phases complement the recommended scheme submitted by Brown-Peterson et al. (2011), who call for a standardization of terminology for describing reproductive development of fishes

Lesão do esmalte após remoção de adesivo ortodontico por pedra de Arkansas e pontas laminadas de carbeto de tungsténio

Objectives: The main aim of this study was to compare the effectiveness of two different methods to remove orthodontic composite adhesives from enamel concerning the surface damage and remnant composite adhesive on the surfaces. Methods: Human molars were stored in buffer solution at room temperature before bonding the brackets. Teeth were ultrasonically cleaned in distilled water before bonding procedure. Ninety two brackets were randomly bonded to the buccal surface of twenty three molars using a composite-based adhesive system. After 15 days, the orthodontic composite adhesives were removed by using Arkansas' stone or multi-blade tungsten burs. After debonding process, the remnant composite adhered to the tooth as well as the teeth surfaces were analyzed by photographic images at x40 magnification concerning the (ARI) adhesive remnant or (SRI) surface roughness index. Also, enamel surfaces were inspected by field emission guns scanning electron microscopy (FEGSEM) before bonding and after bracket detachment. The statistical analysis was performed using SPSS® Statistics vs.18.0, considering a significance level of 0.05 to one-way ANOVA. Tukey's test was used for multiple comparisons and Chi-square tests were used to analyze the association between categorical variables. Results: ARI results revealed no statistically significant differences between the two methods of bracket removal (p=0.283). Considering SRI, statistically significant differences were detected between the two procedures (p<0.001) considering all worn surfaces revealed lower surface roughness after removal of adhesive by Arkansas stone than that recorded on worn surfaces after removal using tungsten carbide burs. Conclusion: The removal of orthodontic adhesive promoted less damage on enamel surfaces by using Arkansas stone at low rotation. Nevertheless, finishing procedures can decrease the roughness on enamel without additional damage.Objetivos: O objetivo deste estudo foi comparar a eficácia de dois métodos diferentes de remocâo do compósito utilizado na adesão de brackets, após a realizacão do tratamento ortodôntico. Métodos: Foram utilizados 92 brackets colados em 23 molares previamente selecionados de acordo com os critérios de inclusão/exclusão. Uma vez removidos os brackets, foram então utilizados os dois métodos de remocão de compósito: a) pedras de Arkansas; b) brocas multilaminadas de tungsténio, ambas utilizadas em contra-ângulo (baixa rotacão). Uma vez removido o compósito, foram analisadas e quantificadas as possíveis lesões advindas do procedimento. A área de compósito remanescente foi calculada em todos os dentes. A aná- lise estatística foi realizada utilizando o SPSS® Statistics vs.18.0, considerando um nível de significância de 0,05 para teste ANOVA. O teste de Tukey foi utilizado para comparações múltiplas e Qui-quadrado para análise entre variáveis categóricas. Resultados: Após a remocão do compósito com cada um dos métodos verificou-se que, relativamente ao índice adesivo remanescente (IAR), não existiam diferença estatisticamente significativa (p=0,283) entre métodos de remoção. Entretanto, diferenças em relação ao índice de rugosidade de superfície (IRS) foram estatisticamente significativas (p<0,001) com resultados a favor do método utilizando pedras de Arkansas. Conclusão: Menor dano ao esmalte foi promovido pela remocão de adesivo ortodóntico com uso da pedra de Arkansas. Entretanto, polimento adicional diminui a rugosidade da superfície sem danos adicionais ao esmalte.This work has been supported by FCT (Fundação para a Ciência e Tecnologia – Portugal) in the scope of the project UID/ EEA/04436/ 2013 NORTE-01-0145- FEDER-000018 - HAMaBIC

Evidence of association of the NLRP1 gene with giant cell arteritis

Recent studies have focused attention on the involvement of NLRP1 to confer susceptibility for extended autoimmune/inflammatory disorders, being considered a common risk factor in autoimmunity. NLRP1 provides a scaffold for the assembly of the inflammasome that activates caspases 1 and 5, required for processing and activation of the proinflammatory cytokines interleukin 1β (IL-1β), IL-18 and IL-33 and promoting inflammation

Identification of the PTPN22 functional variant R620W as susceptibility genetic factor for giant cell arteritis

Objective: To analyse the role of the PTPN22 and CSK genes, previously associated with autoimmunity, in the predisposition and clinical phenotypes of giant cell arteritis (GCA). Methods: Our study population was composed of 911 patients diagnosed with biopsy-proven GCA and 8136 unaffected controls from a Spanish discovery cohort and three additional independent replication cohorts from Germany, Norway and the UK. Two functional PTPN22 polymorphisms (rs2476601/R620W and rs33996649/R263Q) and two variants of the CSK gene (rs1378942 and rs34933034) were genotyped using predesigned TaqMan assays. Results: The analysis of the discovery cohort provided evidence of association of PTPN22 rs2476601/R620W with GCA (PFDR=1.06E-04, OR=1.62, CI 95% 1.29 to 2.04). The association did not appear to follow a specific GCA subphenotype. No statistically significant differences between allele frequencies for the other PTPN22 and CSK genetic variants were evident either in the case/control or in stratified case analysis. To confirm the detected PTPN22 association, three replication cohorts were genotyped, and a consistent association between the PTPN22 rs2476601/R620W variant and GCA was evident in the overall meta-analysis (PMH=2.00E-06, OR=1.51, CI 95% 1.28 to 1.79). Conclusions: Our results suggest that the PTPN22 polymorphism rs2476601/R620W plays an important role in the genetic risk to GCA

In vitro characterisation of fresh and frozen sex-sorted bull spermatozoa

peer-reviewedThis study sought to compare the in vitro characteristics of fresh and frozen non-sorted (NS) and sex-sorted (SS) bull spermatozoa. Experiment 1: Holstein–Friesian ejaculates (n = 10 bulls) were split across four treatments and processed: (1) NS fresh at 3 × 106 spermatozoa, (2) X-SS frozen at 2 × 106 spermatozoa, (3) X-SS fresh at 2 × 106 spermatozoa and (4) X-SS fresh at 1 × 106 spermatozoa. NS frozen controls of 20 × 106 spermatozoa per straw were sourced from previously frozen ejaculates (n = 3 bulls). Experiment 2: Aberdeen Angus ejaculates (n = 4 bulls) were split across four treatments and processed as: (1) NS fresh 3 × 106 spermatozoa, (2) Y-SS fresh at 1 × 106 spermatozoa, (3) Y-SS fresh at 2 × 106 spermatozoa and (4) X-SS fresh at 2 × 106 spermatozoa. Controls were sourced as per Experiment 1. In vitro assessments for progressive linear motility, acrosomal status and oxidative stress were carried out on Days 1, 2 and 3 after sorting (Day 0 = day of sorting. In both experiments SS fresh treatments had higher levels of agglutination in comparison to the NS fresh (P < 0.001), NS frozen treatments had the greatest PLM (P < 0.05) and NS spermatozoa exhibited higher levels of superoxide anion production compared with SS spermatozoa (P < 0.05). Experiment 1 found both fresh and frozen SS treatments had higher levels of viable acrosome-intact spermatozoa compared with the NS frozen treatments (P < 0.01).ACCEPTEDpeer-reviewe

A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis

Giant cell arteritis (GCA) is the most common form of vasculitis in individuals older than 50 years in Western countries. To shed light onto the genetic background influencing susceptibility for GCA, we performed a genome-wide association screening in a well-powered study cohort. After imputation, 1,844,133 genetic variants were analysed in 2,134 cases and 9,125 unaffected controls from ten independent populations of European ancestry. Our data confirmed HLA class II as the strongest associated region (independent signals: rs9268905, P = 1.94E-54, per-allele OR = 1.79; and rs9275592, P = 1.14E-40, OR = 2.08). Additionally, PLG and P4HA2 were identified as GCA risk genes at the genome-wide level of significance (rs4252134, P = 1.23E-10, OR = 1.28; and rs128738, P = 4.60E-09, OR = 1.32, respectively). Interestingly, we observed that the association peaks overlapped with different regulatory elements related to cell types and tissues involved in the pathophysiology of GCA. PLG and P4HA2 are involved in vascular remodelling and angiogenesis, suggesting a high relevance of these processes for the pathogenic mechanisms underlying this type of vasculitis

Analysis of the common genetic component of large-vessel vasculitides through a meta- Immunochip strategy

Giant cell arteritis (GCA) and Takayasu's arteritis (TAK) are major forms of large-vessel vasculitis (LVV) that share clinical features. To evaluate their genetic similarities, we analysed Immunochip genotyping data from 1,434 LVV patients and 3,814 unaffected controls. Genetic pleiotropy was also estimated. The HLA region harboured the main disease-specific associations. GCA was mostly associated with class II genes (HLA-DRB1/HLA-DQA1) whereas TAK was mostly associated with class I genes (HLA-B/MICA). Both the statistical significance and effect size of the HLA signals were considerably reduced in the cross-disease meta-analysis in comparison with the analysis of GCA and TAK separately. Consequently, no significant genetic correlation between these two diseases was observed when HLA variants were tested. Outside the HLA region, only one polymorphism located nearby the IL12B gene surpassed the study-wide significance threshold in the meta-analysis of the discovery datasets (rs755374, P?=?7.54E-07; ORGCA?=?1.19, ORTAK?=?1.50). This marker was confirmed as novel GCA risk factor using four additional cohorts (PGCA?=?5.52E-04, ORGCA?=?1.16). Taken together, our results provide evidence of strong genetic differences between GCA and TAK in the HLA. Outside this region, common susceptibility factors were suggested, especially within the IL12B locus