967 resultados para Blocks of brick
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PURPOSE: Mutations within the KRAS proto-oncogene have predictive value but are of uncertain prognostic value in the treatment of advanced colorectal cancer. We took advantage of PETACC-3, an adjuvant trial with 3,278 patients with stage II to III colon cancer, to evaluate the prognostic value of KRAS and BRAF tumor mutation status in this setting. PATIENTS AND METHODS: Formalin-fixed paraffin-embedded tissue blocks (n = 1,564) were prospectively collected and DNA was extracted from tissue sections from 1,404 cases. Planned analysis of KRAS exon 2 and BRAF exon 15 mutations was performed by allele-specific real-time polymerase chain reaction. Survival analyses were based on univariate and multivariate proportional hazard regression models. RESULTS: KRAS and BRAF tumor mutation rates were 37.0% and 7.9%, respectively, and were not significantly different according to tumor stage. In a multivariate analysis containing stage, tumor site, nodal status, sex, age, grade, and microsatellite instability (MSI) status, KRAS mutation was associated with grade (P = .0016), while BRAF mutation was significantly associated with female sex (P = .017), and highly significantly associated with right-sided tumors, older age, high grade, and MSI-high tumors (all P < 10(-4)). In univariate and multivariate analysis, KRAS mutations did not have a major prognostic value regarding relapse-free survival (RFS) or overall survival (OS). BRAF mutation was not prognostic for RFS, but was for OS, particularly in patients with MSI-low (MSI-L) and stable (MSI-S) tumors (hazard ratio, 2.2; 95% CI, 1.4 to 3.4; P = .0003). CONCLUSION: In stage II-III colon cancer, the KRAS mutation status does not have major prognostic value. BRAF is prognostic for OS in MS-L/S tumors.
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Necrotizing fasciitis is a rare, rapidly spreading, deep-seated infection causing thrombosis of the blood vessels located in the fascia. Necrotizing fasciitis is a surgical emergency. The diagnosis typically relies on clinical findings of severe sepsis and intense pain, although subacute forms may be difficult to recognize. Imaging studies can help to differentiate necrotizing fasciitis from infections located more superficially (dermohypodermitis). The presence of gas within the necrotized fasciae is characteristic but may be lacking. The main finding is thickening of the deep fasciae due to fluid accumulation and reactive hyperemia, which can be visualized using computed tomography and, above all, magnetic resonance imaging (high signal on contrast-enhanced T1 images and T2 images, best seen with fat saturation). These findings lack specificity, as they can be seen in non-necrotizing fasciitis and even in non-inflammatory conditions. Signs that support a diagnosis of necrotizing fasciitis include extensive involvement of the deep intermuscular fascias (high sensitivity but low specificity), thickening to more than 3mm, and partial or complete absence on post-gadolinium images of signal enhancement of the thickened fasciae (fairly high sensitivity and specificity). Ultrasonography is not recommended in adults, as the infiltration of the hypodermis blocks ultrasound transmission. Thus, imaging studies in patients with necrotizing fasciitis may be challenging to interpret. Although imaging may help to confirm deep tissue involvement and to evaluate lesion spread, it should never delay emergency surgical treatment in patients with established necrotizing fasciitis.
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Pieces of Iowas Past, published by the Iowa State Capitol Tour Guides weekly during the legislative session, features historical facts about Iowa, the Capitol, and the early workings of state government. All historical publications are reproduced here with the actual spelling, punctuation, and grammar retained. February 20, 2008 THIS WEEK: The Old Brick Capitol
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Owing to its high fat content, the classical Western diet has a range of adverse effects on the heart, including enhanced inflammation, hypertrophy, and contractile dysfunction. Proinflammatory factors secreted by cardiac cells, which are under the transcriptional control of nuclear factor-κB (NF-κB), may contribute to heart failure and dilated cardiomyopathy. The underlying mechanisms are complex, since they are linked to systemic metabolic abnormalities and changes in cardiomyocyte phenotype. Peroxisome proliferator-activated receptors (PPARs) are transcription factors that regulate metabolism and are capable of limiting myocardial inflammation and hypertrophy via inhibition of NF-κB. Since PPARβ/δ is the most prevalent PPAR isoform in the heart, we analyzed the effects of the PPARβ/δ agonist GW501516 on inflammatory parameters. A high-fat diet induced the expression of tumor necrosis factor-α, monocyte chemoattractant protein-1, and interleukin-6, and enhanced the activity of NF-κB in the heart of mice. GW501516 abrogated this enhanced proinflammatory profile. Similar results were obtained when human cardiac AC16 cells exposed to palmitate were coincubated with GW501516. PPARβ/δ activation by GW501516 enhanced the physical interaction between PPARβ/δ and p65, which suggests that this mechanism may also interfere NF-κB transactivation capacity in the heart. GW501516-induced PPARβ/δ activation can attenuate the inflammatory response induced in human cardiac AC16 cells exposed to the saturated fatty acid palmitate and in mice fed a high-fat diet. This is relevant, especially taking into account that PPARβ/δ has been postulated as a potential target in the treatment of obesity and the insulin resistance state.
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Pieces of Iowas Past, published by the Iowa State Capitol Tour Guides weekly during the legislative session, features historical facts about Iowa, the Capitol, and the early workings of state government. All historical publications are reproduced here with the actual spelling, punctuation, and grammar retained. January 11, 2012 THIS WEEK: PROFESSORSHIPS AND STUDENT ENROLLMENT AT THE STATE UNIVERSITY BACKGROUND: The Ninth General Assembly convened January 13, 1862, and adjourned April 8, 1862an 86-day session. The Brick Capitol in Des Moines had been the seat of government for four years. John R. Needham was the Lt. Governor presiding in the Senate, and Rush Clark was the Speaker of the House of Representatives. The Republican Party had the majority in both the House of Representatives and the Senate. The legislature had 140 members. Samuel Kirkwood was the governor, serving his second term. Governor Kirkwood was the first governor of Iowa to be re-elected to a second term and the first governor to serve nonconsecutive terms. He was 46 at the time of his first Inaugural on January 11, 1860. The 1860 census showed Iowas population at 674,913.
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Pieces of Iowas Past, published by the Iowa State Capitol Tour Guides weekly during the legislative session, features historical facts about Iowa, the Capitol, and the early workings of state government. All historical publications are reproduced here with the actual spelling, punctuation, and grammar retained. February 8, 2012 THIS WEEK: The Resolution Granting a Festival for the Citizens of Des Moines BACKGROUND: The following comes from a journal entry in the Pioneer Lawmakers Association of Iowa, Volumes 1-14, 1896-1913. The journal entry is from the Third Annual Meeting of the Pioneer Lawmakers Reunion of 1892. The president, Charles Aldrich, called the meeting to order February 10, 1892, in the assembly rooms of the Young Mens Christian Association. Governor Cyrus Carpenter gave the address. Cyrus Carpenter was born November 24, 1829, and died May 29, 1898. He served in the Seventh General Assembly in 1858. This was the first general assembly to meet in Des Moines in the newly constructed Brick Capitol. Carpenter was Iowas eighth governor since becoming a state in 1846. He was inaugurated in 1872 at the age of 42. Carpenter also served in the Iowa Senate during the 20th General Assembly in 1884
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Pieces of Iowas Past, published by the Iowa State Capitol Tour Guides weekly during the legislative session, features historical facts about Iowa, the Capitol, and the early workings of state government. All historical publications are reproduced here with the actual spelling, punctuation, and grammar retained. January 23, 2013 THIS WEEK: Iowas Grasshopper Plague of 1873 BACKGROUND: Fifteen General Assembly The 15th General Assembly convened January 12 and adjourned March 19, 1874a 67-day session. The Senate had six Democratic members, 34 Republican members, and 10 Independent members. The House of Representatives had six Democratic members, 50 Republican members, and 44 Independent members. There were a total of 150 legislators in Iowa. By 1874, the Capital had been relocated to Des Moines. The legislature had occupied the old Brick Capitol since 1858. Joseph Dysart was the Lieutenant Governor presiding in the Senate, and John Gear was Speaker of the House of Representatives. Iowas population at the 1870 federal census had grown to 1,194,020. Both House and Senate journals from the 15th Iowa General Assembly include several references to assisting the destitution brought on by the 1874 plague of grasshoppers in Northwestern Iowa. Senator Perkins, from the Special Committee appointed to inquire into the reports of destitution in the northwestern counties of Iowa, submitted the following report, in part: We have examined such evidence as is attainable here, and made such inquiries of parties interested in affording temporary relief as were to be met, and are pieces satisfied in our own minds that the case is one of sufficient importance to command the attention of the State.
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ABSTRACT The network of actin cytoskeleton is composed of actin filaments (F-actin) that are made by polymerisation of actin monomers and actin binding proteins. It is required for growth and morphogenesis of eukaryotic cells. The labelling of F-actin with constitutively expressed GFP-Talin (Kost et al., 1998) reveals the organisation of cellular actin networks in plants. Due to the lack of information on actin cytoskeleton through gametophytic development of the model moss plant Physcornitrella patens, stable transgenic lines overexpressing GFP-Talin were generated to detect F-actin structures. It is shown that the 35S promoter driven expression is not suitable for F-actin labelling in all cells. When it is replaced by the inducible heat-shock promoter Gmhsp17.3 from soybean, one hour mild heat stress at 37C followed by recovery at 25C is enough to induce efficient and transient labelling in all tissues without altering cellular morphology. The optimal observations of F-actin structures at different stages of moss development can be done between 12-18 hours after the induction. By using confocal microscopy, we demonstrate that stellated actin arrays were densely accumulated at the growing tip in regenerating protoplasts, apical protonemal cells and rhizoids and connected with a fine dispersed F-actin mesh. Following three-dimensional growth, the cortical star-like structures are widespread in the meristematic cells of developing bud and young gametophores. On the contrary, undulating networks of actin cables are found at the final stage of cell differentiation. During redifferentiation of mature leaf cells into protonemal filaments the rather stagnant web of actin cables is replaced by diffuse actin meshwork. In eukaryotes, nucleation of the actin monomers prior to their polymerization is driven by the seven-subunit ARP2/3 complex and formins. We cloned the gene encoding the ARP3 subunit of P. patens and generated arp3 mutants of the moss through gene disruption. The knockout of ARP3 affects the elongation of chloronemal cells and blocks further differentiation of caulonemal cells and rhizoids, and the gametophores are slightly stunted compared to wild-type. The arp mutants were created in the heat-shock inducible GFP-Talin strains allowing us to visualise a disorganised actin network and a lack of star-like actin cytoskeleton arrays. We conclude that ARP2/3 dependent nucleation of actin filaments is critical for the growth of filamentous cells, which in turn influences moss colonization. In complementation assays, the overexpression of Physcomitrella and Arab idopsis ARP3 genes in the moss arp3 mutant results in full recovery of wild type phenotype. In contrast the ARP3 subunit of fission yeast is not able to complement the moss arp3 mutant of moss indicating that regulation of the ARP2/3 dependent actin nucleation diverged in different kingdoms. RESUME Le rseau d'actine est compos de filaments de F-actine et d'un ensemble de protines s'y attachant (Actin binding proteins). Le rseau d'actine est ncessaire la croissance et la morphogense de toutes les cellules eucaryotes. Chez les plantes, le marquage ainsi que l'tude de l'organisation du rseau d'actine ont t raliss en utilisant une fusion GFP-Talin (Kost et al., 1998) exprime sous le control d'un promoteur constitutif. Afin d'tudier les structures F-actine dans les cellules de Physcomitrella Patens et pour combler le manque d'information sur le dveloppement des gamtophores, des lignes transgniques stables surexprimant GFP-Talin ont t cres. Nous avons dmontr que l'utilisation du promoteur 35S est inadquate pour le marquage complet et homogne des filaments d'actine dans toutes les cellules de P. patens. Par contre, l'utilisation du promoteur inductible Gmhsp17.3 nous a permis de raliser un marquage transitoire et gnral dans tous les tissus de la mousse. Une heure de choc thermique 37C suivis d'un temps de rcupration de 12-18h 25C sont les conditions optimales (sans dommages cellulaires) pour l'observation des structures F-actine diffrentes tapes de dveloppement de la mousse. En utilisant la microscopie confocale, nous avons observ l'existence de structures F-actine accumules en forme d'toiles. Ces structures, qui sont lies au rseau de microfilaments d'actine, ont t observes dans les protoplastes en rgnration, les cellules des protonema apicales ainsi que dans les rhizodes. En suivant la croissance tridimensionnelle, ces structures en toiles ont t observes dans les cellules meristmatiques des bourgeons et des jeunes gamtophores. Par contre, dans les cellules diffrenties ces structures laissent place des rseaux de cbles pais. Nous avons galement remarqu que durant la redifferentiation des cellules foliaires le rseau de cbles de F-actine est remplac par un rseau de F-actine diffus. Dans les cellules eucaryotes, la nuclation des filaments d'actirie prcdant leur polymrisation est contrl par sept sous units du complexe ARP2/3 et par des formines. Nous avons isol le gne codant pour la sous unit ARP3 de P. patens et nous avons cre des mutants arp3 par intgration cible (Knockout). L'longation des cellules chloronema est clairement affecte dans les mutants arp3. La diffrentiation des caulonemata et des rhizodes est bloque et les gametophores sont lgrement plus courts compar au type sauvage. A fin d'tudier l'organisation des filaments d'actines dans les mutants arp3, nous avons aussi ralis un arp3-knockout dans la ligne Hsp-GFP-Talin. La nouvelle ligne gnre nous a permis de visualiser une dsorganisation du rseau d'actine et une absence complte de structures de F-actine accumule en forme d'toiles. Les rsultats obtenus nous amnent conclure que la nuclation (ARP2/3 dpendante) des filaments d'actine est indispensable la croissance des cellules filamenteuses. Par consquent, les filaments d'actine semblent avoir un rle dans la colonisation des milieux par les mousses. Nous avons galement procd des essais de complmentation du mutant arp3. La surexpression des gnes ARP3 de Physcomitrella et d'Arabidopsis dans les cellules du mutant arp3 rtabli compltement le phnotype WT. Par contre, le gne ARP3 des levures n'est pas suffisant pour complmenter la mme mutation dans les cellules de mousses. Ce rsultat dmontre que les mcanismes de rgulation de la nuclation des filaments d'actine (ARP2/3 dpendante) sont diffrents entre les diffrents groupes d'eucaryotes.
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BACKGROUND: Multislice CT (MSCT) combined with D-dimer measurement can safely exclude pulmonary embolism in patients with a low or intermediate clinical probability of this disease. We compared this combination with a strategy in which both a negative venous ultrasonography of the leg and MSCT were needed to exclude pulmonary embolism. METHODS: We included 1819 consecutive outpatients with clinically suspected pulmonary embolism in a multicentre non-inferiority randomised controlled trial comparing two strategies: clinical probability assessment and either D-dimer measurement and MSCT (DD-CT strategy [n=903]) or D-dimer measurement, venous compression ultrasonography of the leg, and MSCT (DD-US-CT strategy [n=916]). Randomisation was by computer-generated blocks with stratification according to centre. Patients with a high clinical probability according to the revised Geneva score and a negative work-up for pulmonary embolism were further investigated in both groups. The primary outcome was the 3-month thromboembolic risk in patients who were left untreated on the basis of the exclusion of pulmonary embolism by diagnostic strategy. Clinicians assessing outcome were blinded to group assignment. Analysis was per protocol. This study is registered with ClinicalTrials.gov, number NCT00117169. FINDINGS: The prevalence of pulmonary embolism was 20.6% in both groups (189 cases in DD-US-CT group and 186 in DD-CT group). We analysed 855 patients in the DD-US-CT group and 838 in the DD-CT group per protocol. The 3-month thromboembolic risk was 0.3% (95% CI 0.1-1.1) in the DD-US-CT group and 0.3% (0.1-1.2) in the DD-CT group (difference 0.0% [-0.9 to 0.8]). In the DD-US-CT group, ultrasonography showed a deep-venous thrombosis in 53 (9% [7-12]) of 574 patients, and thus MSCT was not undertaken. INTERPRETATION: The strategy combining D-dimer and MSCT is as safe as the strategy using D-dimer followed by venous compression ultrasonography of the leg and MSCT for exclusion of pulmonary embolism. An ultrasound could be of use in patients with a contraindication to CT.
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Arenaviruses are enveloped negative single strand RNA viruses that include a number of important human pathogens. The most prevalent human pathogen among the arenaviruses is the Old World arenavirus Lassa virus (LASV) which is endemic in West Africa from Senegal to Cameroon. LASV is the etiologic agent of a severe viral hemorrhagic fever named Lassa fever whose mortality rate can reach 30% in hospitalized patients. One of the hallmarks of fatal arenavirus infection in humans is the absence of an effective innate and adaptive immune response. In nature, arenaviruses are carried by rodents which represent the natural reservoirs as well as the vectors for transmission. In their natural rodent reservoir, arenaviruses have the ability to establish persistent infection without any overt signs and symptoms of pathology. We believe that the modulation of the host cell's innate immunity by arenaviruses is a key determinant for persistence in the natural host and for the pathogenesis in man. In this thesis, we studied the interaction of arenaviruses with two main branches of the host's innate anti-viral defense, the type I interferon (IFN) system and virus-induced mitochondrial apoptosis. The arenavirus nucleoprotein (NP) is responsible for the anti-IFN activity of arenaviruses. Specifically, NP blocks the activation and the nuclear translocation of the transcription factor interferon regulatory factor 3 (IRF3) which leads to type I IFN production. LASV and the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) NPs contain a 3'-5'exoribonuclease domain in the C terminal part that has been linked to the anti-IFN activity of NP. In the first project, we sought to identify cellular component(s) of the type I IFN induction pathway targeted by the viral NP. Our study revealed that LCMV NP prevents the activation of IRF3 by blocking phosphorylation of the transcription factor. We found that LCMV NP specifically targets the IRF-activating kinase IKKs, and this specific binding is conserved within the Arenaviridae. We could also demonstrate that LCMV NP associates with the kinase domain of IKKs involving NP's C-terminal region. Lastly, we showed that the binding of LCMV NP inhibits the kinase activity of IKKs. This study allowed the discovery of a new cellular interacting partner of arenavirus NP. This newly described association may play a role in the anti-IFN activity of arenaviruses but potentially also in other aspects of arenavirus infection. For the second project, we investigated the ability of arenaviruses to avoid and/or suppress mitochondrial apoptosis. As persistent viruses, arenaviruses evolved a "hit and stay" survival strategy where the apoptosis of the host cell would be deleterious. We found that LCMV does not induce mitochondrial apoptosis at any time during infection. Specifically, no caspase activity, no cytochrome c release from the mitochondria as well as no cleavage of poly (ADP-ribose) polymerase (PARP) were detected during LCMV infection. Interestingly, we found that virus-induced mitochondrial apoptosis remains fully functional in LCMV infected cells, while the induction of type IIFN is blocked. Since both type IIFN production and virus- induced mitochondrial apoptosis critically depend on the pattern recognition receptor (PRR) RIG-I, we examined the role of RIG-I in apoptosis in LCMV infected cells. Notably, virus- induced mitochondrial apoptosis in LCMV infected cells was found to be independent of RIG- I and MDA5, but still depended on MAVS. Our study uncovered a novel mechanism by which arenaviruses alter the host cell's pro-apoptotic signaling pathway. This might represent a strategy arenaviruses developed to maintain this branch of the innate anti-viral defense in absence of type I IFN response. Taken together, these results allow a better understanding of the interaction of arenaviruses with the host cell's innate immunity, contributing to our knowledge about pathogenic properties of these important viruses. A better comprehension of arenavirus virulence may open new avenues for vaccine development and may suggest new antiviral targets for therapeutic intervention against arenavirus infections. - Les arenavirus sont des virus envelopps ARN simple brin qui comportent un grand nombre de pathognes humains. Le pathogne humain le plus important parmi les arenavirus est le virus de Lassa qui est endmique en Afrique de l'Ouest, du Sngal au Cameroun. Le virus de Lassa est l'agent tiologique d'une fivre hmorragique svre appele fivre de Lassa, et dont le taux de mortalit peut atteindre 30% chez les patients hospitaliss. L'une des caractristiques principales des infections fatales arenavirus chez l'Homme est l'absence de rponse immunitaire inne et adaptative. Dans la nature, les arenavirus sont hbergs par diffrentes espces de rongeur, qui reprsentent la fois les rservoirs naturels et les vecteurs de transmission des arenavirus. Dans leur hte naturel, les arenavirus ont la capacit d'tablir une infection persistante sans symptme manifeste d'une quelconque pathologie. Nous pensons que la modulation de systme immunitaire inn de la cellule hte par les arenavirus est un paramtre cl pour la persistance au sein de l'hte naturel, ainsi que pour la pathogense chez l'Homme. L'objectif de cette thse tait d'tudier l'interaction des arenavirus avec deux branches essentielles de la dfense antivirale inne de la cellule hte, le systme interfron (IFN) de type I et l'apoptose. La nucloprotine virale (NP) est responsable de l'activit anti-IFN des arenavirus. Plus spcifiquement, la NP bloque 1'activation et la translocation nuclaire du facteur de transcription IRF3 qui conduit la production des IFNs de type I. La NP du virus de Lassa et celle du virus de la choriomningite lymphocytaire (LCMV), l'arnavirus prototypique, possdent dans leur extrmit C-terminale un domaine 3'-5' exoribonuclase qui a t associ l'activit anti-IFN de ces protines. Dans un premier projet, nous avons cherch identifier des composants cellulaires de la cascade de signalisation induisant la production d'IFNs de type I qui pourraient tre cibls par la NP virale. Nos recherches ont rvl que la NP de LCMV empche 1'activation d'IRF3 en bloquant la phosphorylation du facteur de transcription. Nous avons dcouvert que la NP de LCMV cible spcifiquement la kinase IKKe, et que cette interaction spcifique est conserve travers la famille des Arenaviridae. Notre tude a aussi permis de dmontrer que la NP de LCMV interagit avec le domaine kinase d'IKKe et que l'extrmit C-terminale de la NP est implique. Pour finir, nous avons pu tablir que l'association avec la NP de LCMV inhibe l'activit kinase d'IKKe. Cette premire tude prsente la dcouverte d'un nouveau facteur cellulaire d'interaction avec la NP des arenavirus. Cette association pourrait jouer un rle dans l'activit anti-IFN des arnavirus, mais aussi potentiellement dans d'autres aspects des infections arnavirus. Pour le second projet, nous nous sommes intresss la capacit des arnavirus viter et/ou supprimer l'apoptose mitochondriale. En tant que virus persistants, les arnavirus ont volu vers une stratgie de survie "hit and stay" pour laquelle l'apoptose de la cellule hte serait nfaste. Nous avons observ qu' aucun moment durant l'infection LCMV n'induit l'apoptose mitochondriale. Spcifiquement, aucune activit de caspase, aucune libration mitochondriale de cytochrome c ainsi qu'aucun clivage de la polymerase poly(ADP-ribose) (PARP) n'a t dtect pendant l'infection LCMV. Il est intressant de noter que l'apoptose mitochondriale induite par les virus reste parfaitement fonctionnelle dans les cellules infectes par LCMV, alors que l'induction de la rponse IFN de type I est bloque dans les mmes cellules. La production des IFNs de type I et l'apoptose mitochondriale induite par les virus dpendent toutes deux du rcepteur de reconnaissance de motifs molculaires RIG-I. Nous avons, par consquent, investigu le rle de RIG-I dans l'apoptose qui a lieu dans les cellules infectes par LCMV lorsqu'on les surinfecte avec un autre virus pro-apoptotique. En particulier, l'apoptose mitochondriale induite par les surinfections s'est rvle indpendante de RIG-I et MDA5, mais dpendante de MAVS dans les cellules prcdemment infectes par LCMV. Notre tude dmontre ainsi l'existence d'un nouveau mcanisme par lequel les arnavirus altrent la cascade de signalisation pro-apoptotique de la cellule hte. Il est possible que les arnavirus aient dvelopp une stratgie permettant de maintenir fonctionnelle cette branche de la dfense antivirale inne en l'absence de rponse IFN de type I. En conclusion, ces rsultats nous amnent mieux comprendre l'interaction des arnavirus avec l'immunit inne de la cellule hte, ce qui contribue aussi amliorer notre connaissance des proprits pathogniques de ces virus. Une meilleure comprhension des facteurs de virulence des arnavirus permet, d'une part, le dveloppement de vaccins et peut, d'autre part, servir de base pour la dcouverte de nouvelles cibles thrapeutiques utilises dans le traitement des infections arnavirus.
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Many researchers have concluded that secondary or delayed ettringite is responsible for serious premature deterioration of concrete highways. In some poorly performing Iowa concretes, ettringite is the most common secondary mineral but its role in premature deterioration is uncertain since some researchers still maintain that secondary ettringite does not itself cause deterioration. The current research project was designed to determine experimentally if it is possible to reduce secondary ettringite formation in concrete by treating the concrete with commercial crystallization inhibitor chemicals. The hypothesis is such that if the amount of ettringite is reduced, there will also be a concomitant reduction of concrete expansion and cracking. If both ettringite formation and deterioration are simultaneously reduced, then the case for ettringite induced expansion/cracking is strengthened. The experiment used four commercial inhibitors - two phosphonates, a polyacrylic acid, and a phosphate ester. Concrete blocks were subjected to continuous immersion, wet/dry and freeze/thaw cycling in sodium sulfate solutions and in sulfate solutions containing an inhibitor. The two phosphonate inhibitors, Dequest 2060 and Dequest 2010, manufactured by Monsanto Co., were effective in reducing ettringite nucleation and growth in concrete. Two other inhibitors, Good-rite K752 and Wayhib S were somewhat effective, but less so than the two phosphonates. Rapid experiments with solution growth inhibition of ettringite without the presence of concrete phases were used to explore the mechanisms of inhibition of this mineral. Reduction of new ettringite formation in concrete blocks also reduced expansion and cracking of the blocks. This relationship clearly links concrete expansion with this mineral - a conclusion that some research workers have disputed despite theoretical arguments for such a relationship and despite numerous observations of ettringite mineralization in prematurely deteriorated concrete highways. Secondary ettringite nucleation and growth must cause concrete expansion because the only known effect of the inhibitor chemicals is to reduce crystal nucleation and growth, and the inhibitors cannot in any other way be responsible for the reduction in expansion. The mechanism of operation of the inhibitors on ettringite reduction is not entirely clear but the solution growth experiments show that they prevent crystallization of a soluble ettringite precursor gel. The present study shows that ettringite growth alone is not responsible for expansion cracking because the experiments showed that most expansion occurs under wet/dry cycling, less under freeze/thaw cycling, and least under continuous soaking conditions. It was concluded from the different amounts of damage that water absorption by newly-formed, minute ettringite crystals is responsible for part of the observed expansion under wet/dry conditions, and that reduction of freeze resistance by ettringite filling of air-entrainment voids is also important in freeze/thaw environments.
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The formation and structural evolution of the jungrau syncline is described, based on excellent outcrops occurring in the lotschental, in the central alps of switzerland. the quality of the outcrops allows us to demonstrate that the external massifs of the swiss alps have developed due to internal folding. The jungfrau suncline, which separates the autochtonous gastern dome from the aar massif basement gneiss folds, is composed of slivers of basement rocks with their mesozoic sedimentary cover. in the inner faflertal, a side valley of the lotschental, the 200 m thick syncline cp, roses fpir imots, the gastern massif with a reduced mesozoic sedimentary cover in a normal stratigraphic succession, two units of overturned basement rocks with their mesozoic sedimentary cover, and the overturned lower limn of the tschingelhorn gneiss fold of the aar massif with lenses of its sedimentary cover. stratigraphy shows that the lower units, related to the gastern massis, are condensed and that the upper units, deposited farther away from a gastern paleo-high, form a more complete sequence, linked to the doldenhorn meso-cneozoic basin fill. the integration of these local observations with published regional data leads to the following model. on the northern margin of the doldenhorn hbasin, at the northern fringe of the alpine tethuys, the pre-triassic crystalline basement and its mesozoic sedimentary cover were folded by ductile deformation at temperatures above 300 degrees C and in the presence of high fluid pressures, as the helveti c and penninic nappes were overthrusted towards the northwest during the main alpine deformation phase, the visosity contrast between the basement gneisses and the sediments caused the formation of large basement anticlines and tight sedimentary sunclines (mullion-type structures). The edges of basement blocks bounded buy pre-cursor se-dipping normal faults at the northwestern border of the doldenhorn basin were deformed bu simple shear, creating overturned slices of crystalline rocks with their sedimentary cover in what now forms the hungfrau syncline. the localisation of ductile deformation in the vicinity of pre-existing se-dipping faults is thought to have been helped by the circulation of fluids along the faults; these fluids would have been released from the mesozoic sediments by metamorphic dehydration reactions accompanied by creep and dynamic recrystallisation of quartz at temperatures above 300 degrees C. Quantification of the deformation suggests an strain ellipsoid with a ratio (1 + e(1)/+ e(3)) of approximately 1000. The jungfrau suncline was deformed bu more brittle nw-directed shear creating well-developed shear band cleavages at a late stage, after cooling by uplift and erosion. It is suggested that the external massifs of the apls are basement gneiss folds created at temperatures of 300 degrees C by detachment through ductile deformation of the upper crust of the european plate as it was underthrusted below the adriatic plate.
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Two trials were performed in Balcarce, Argentina (37 45' LS; 58 18' LW) during 1993-94, to assess the effect of eight herbicides applied individually or in tank mixtures, on nodule number, nodule dry weight, seed yield and N percent in seed in soybean Asgrow 3205, inoculated with Bradyrhizobium japonicum CB 1809. Individual herbicides and doses in kg ha-1 of a.i. were metribuzin (0.48), acetochlor (0.90), metolachlor (1), flumioxazin (0.075), trifluralin (0.96), imazaquin (0.20), imazethapyr (0.10) and chlorimuron ethyl (0.0125). The mixtures were metribuzin+acetochlor (0.48+0.9), flumioxazin+acetochlor (0.075+0.9), imazaquin+acetochlor (0.2+0.9), metribuzin+metolachlor (0.48+1.92), and flumioxazin+ metolachlor (0.075+1.92). A control treatment without herbicides was included. Both trials were laid out as randomized complete blocks with four replicates, on a loam illitic thermic petrocalcic Paleudoll, 5.7% organic matter (OM), 25% clay, 30.4 cmol kg-1 CEC. Nodules were sampled at V2 (second node), V6 (sixth node) and R5 (beginning seed) growth stages. Herbicides did not significantly affect the beginning of nodulation or nodule number and mass at R5, not either grain yield or N accumulation. This indicates lack of interference between soil interacting herbicides and N fixation in the high organic matter, loam soils of SE Buenos Aires province, even though a tendency in less number and dry weight of nodules was evident at the two latter growth stages.
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This paper focused on four alternatives of analysis of experiments in square lattice as far as the estimation of variance components and some genetic parameters are concerned: 1) intra-block analysis with adjusted treatment and blocks within unadjusted repetitions; 2) lattice analysis as complete randomized blocks; 3) intrablock analysis with unadjusted treatment and blocks within adjusted repetitions; 4) lattice analysis as complete randomized blocks, by utilizing the adjusted means of treatments, obtained from the analysis with recovery of interblock information, having as mean square of the error the mean effective variance of this same analysis with recovery of inter-block information. For the four alternatives of analysis, the estimators and estimates were obtained for the variance components and heritability coefficients. The classification of material was also studied. The present study suggests that for each experiment and depending of the objectives of the analysis, one should observe which alternative of analysis is preferable, mainly in cases where a negative estimate is obtained for the variance component due to effects of blocks within adjusted repetitions.
Resumo:
We investigated in conscious normotensive rats the effect of SKF64139 (2 mg i.v.), a potent phenylethanolamine N-methyltransferase (PNMT) inhibitor, on blood pressure responses to norepinephrine (40, 80, and 160 ng i.v.); methoxamine (2.5, 5 and 10 micrograms i.v.), a directly active sympathomimetic agent that is not taken up by adrenergic nerves; and tyramine (20, 40, and 80 micrograms i.v.), an indirectly acting sympathomimetic amine. The pressor effect of norepinephrine was not changed by 2 mg of SKF64139, while those of methoxamine and tyramine were significantly reduced. The dose-response curve to exogenous norepinephrine was also evaluated following blockade of norepinephrine uptake in the nerve endings using 0.25 mg desipramine i.v. This dose of desipramine had no effect on blood pressure increase induced by methoxamine. In rats pretreated with the neuronal uptake inhibitor desipramine in a dose that did not affect alpha-adrenoceptors, SKF64139 significantly decreased the pressor responses to norepinephrine. Increasing the dose of SKF64139 to 8 mg i.v. resulted in a significant fall in base-line blood pressure and in a blunted blood pressure response to norepinephrine. These data demonstrate that in vivo the PNMT inhibitor SKF64139 blocks alpha-adrenoceptors and inhibits neuronal uptake. The alpha-adrenoceptor blocking properties of SKF65139 are masked by simultaneous blockade of norepinephrine uptake when agonists with affinity for the uptake system are used. These findings need to be taken into account when interpreting cardiovascular effects of the PNMT inhibitor SKF64139.
