summary This study evaluated the abrasiveness of four denture cleaners on the surface of denture base material and assessed their ability to remove Candida albicans. Acrylic resin discs 20 mm ...diameter and 2 mm thick were identically produced and polished. Four cleaners were evaluated: conventional toothpaste; toothpaste with stain remover; denture cleaning paste and an immersion type cleaner, and water were used as control. These were used at dilutions of 1:1, 1:2 and 1:3 with water. An electric toothbrush was used, and the discs cleaned to simulate 1 years’ cleaning. The surface roughness of the discs were then measured, before and after cleaning, using a stylus profilometer, then inoculated with 1·2 × 106C. albicans cells. The effectiveness of the denture cleaners to remove C. albicans cells was assessed following a single cleaning event. The immersion cleaner was significantly less abrasive than paste cleaners (P < 0·05). There were no significant differences between any dilutions for any cleaner used (P > 0·05). Immersion and paste cleaners removed almost all recoverable C. albicans from the discs, as cleaning with water alone was less effective (P < 0·05). An immersion type cleaner was found to be the most suitable cleaner because of its low abrasivity and effective removal of organic debris.
Nrf1p was first identified in a screen for negative regulators of the Cdc42p GTPase. Overexpression of Nrf1p resulted in dose-dependent lethality, with cells exhibiting an ellipsoidal morphology and ...abnormal vacuolar phenotypes including an increase in vacuolar fusion. Green fluorescent protein (GFP)-Cdc42p and GFP-Nrf1p colocalized to vacuolar membranes and GFP-Nrf1p vacuolar localization depended on Scd1p, the Schizosaccharomyces pombe homolog of the Cdc24p guanine nucleotide exchange factor. In this study, site-directed mutagenesis was conducted on Nrf1p to determine its functional domains. Mutations in the three putative transmembrane domains resulted in mislocalization of GFP-Nrf1p and an inability to induce lethality, suggesting a loss of function. Mutations in the second extramembranous loop of Nrf1p also resulted in a loss of function and altered the ability of GFP-Nrf1p to localize to vacuolar membranes. Analysis of Δnrf1 and Δscd1 mutants revealed defects in endocytosis. In addition, overexpression of constitutively active Cdc42G12Vp resulted in an increase in endocytosis and an ability to rescue the endocytic defects in Δnrf1 and Δscd1 cells. These data are consistent with Nrf1p and Scd1p being necessary for efficient endocytosis, possibly through the regulation of Cdc42p.
More than ever before, as the classroom population increasingly diversifies, educators need a clear, concise guide to designing and implementing responsive curriculum. This book, built around the ...lessons of classroom teachers, provides the "how" of instruction design. Designing Responsive Curriculum details the most important components of design: (1) Addressing standards; (2) Designing multiple assessments; (3) Identifying richly detailed source materials; and (4) Creating interrelated lessons and culminating activities. It also expands on the needs of diverse learners and contains a completed instructional plan, easily adaptable to teachers' content and grade level. The chapters provide readers with additional information on grouping students for instruction, literacy instruction and differentiating instruction. This guide will be helpful to preservice and inservice teachers. This book is organized into the following seven chapters: (1) Standards, Expectations, and Essential Questions; (2) Designing Multiple Formal and Informal Assessments; (3) Identifying Richly Detailed Source Material; (4) Designing Interrelated Daily Lessons and Culminating Activities; (5) Literacy Instruction Across Content Areas; (6) Effective Grouping for Instruction; and (7) Focusing on Diverse Learners.
Abstract
H2O2 is a widespread molecule in many biological systems. It is created enzymatically in living cells during various oxidation reactions and by leakage of electrons from the electron ...transport chains. Depending on the concentration H2O2 can induce cell protective responses, programmed cell death, or necrosis. Here we provide evidence that H2O2 may function as a developmental signal in the differentiation of secondary walls in cotton (Gossypium hirsutum) fibers. Three lines of evidence support this conclusion: (a) the period of H2O2 generation coincided with the onset of secondary wall deposition, (b) inhibition of H2O2 production or scavenging the available H2O2 from the system prevented the wall differentiation process, and (c) exogenous addition of H2O2 prematurely promoted secondary wall formation in young fibers. Furthermore, we provide support for the concept that H2O2 generation could be mediated by the expression of the small GTPase Rac, the accumulation of which was shown previously to be strongly induced during the onset of secondary wall differentiation. In support of Rac's role in the activation of NADPH oxidase and the generation of reactive oxygen species, we transformed soybean (Glycine max) and Arabidopsis cells with mutated Rac genes. Transformation with a dominantly activated cotton Rac13 gene resulted in constitutively higher levels of H2O2, whereas transformation with the antisense and especially with dominant-negative Rac constructs decreased the levels of H2O2.
Measuring environmental variables at appropriate temporal and spatial scales remains an important challenge in ecological research. New developments in wireless sensors and sensor networks will free ...ecologists from a wired world and revolutionize our ability to study ecological systems at relevant scales. In addition, sensor networks can analyze and manipulate the data they collect, thereby moving data processing from the end user to the sensor network itself. Such embedded processing will allow sensor networks to perform data analysis procedures, identify outlier data, alter sampling regimes, and ultimately control experimental infrastructure. We illustrate this capability using a wireless sensor network, the Sensor Web, in a study of microclimate variation under shrubs in the Chihuahuan Desert. Using Sensor Web data, we propose simple analytical protocols for assessing data quality "on-the-fly" that can be programmed into sensor networks. The ecological community can influence the evolution of environmental sensor networks by working across disciplines to infuse new ideas into sensor network development.
Cdc24p is the guanine-nucleotide exchange factor for the Cdc42p GTPase, which controls cell polarity in Saccharomyces cerevisiae. To identify new genes that may affect cell polarity, we characterized ...six UV-induced csl (CDC24 synthetic-lethal) mutants that exhibited synthetic-lethality with cdc24-4ls at 23 degrees. Five mutants were not complemented by plasmid-borne CDC42, RSR1, BUD5, BEM1, BEM2, BEM3 or CLA4 genes, which are known to play a role in cell polarity. The csl3 mutant displayed phenotypes similar to those observed with calcium-sensitive, Pet- vna mutants defective in vacuole function. CSL5 was allelic to VMA5, the vacuolar H(+)-ATPase subunit C, and one third of csl5 cdc24-4ls cells were elongated or had misshapen buds. A cdc24-4ls delta vma5::LEU2 double mutant did not exhibit synthetic lethality, suggesting that the csl5/vma5 cdc24-4ls synthetic-lethality was not simply due to altered vacuole function. The cdc24-4ls mutant, like delta vma5::LEU2 and csl3 mutants, was sensitive to high levels of Ca2+ as well as Na+ in the growth media, which did not appear to be a result of a fragile cell wall because the phenotypes were not remedied by 1 M sorbitol. Our results indicated that Cdc24p was required in one V-ATPase mutant and another mutant affecting vacuole morphology, and also implicated Cdc24p in Na+ tolerance.
The Saccharomyces cerevisiae Cdc42p GTPase is localized to the plasma membrane and involved in signal transduction mechanisms controlling cell polarity.
The mechanisms of action of the dominant ...negative cdc42
D118A mutant and the lethal, gain of function cdc42
G12V mutant were examined. Cdc42 D118A,C188S p and its guanine-nucleotide exchange factor Cdc24p displayed a temperature-dependent interaction in the two-hybrid system,
which correlated with the temperature dependence of the cdc42
D118A phenotype and supported a Cdc24p sequestration model for the mechanism of cdc42
D118A action. Five cdc42 mutations were isolated that led to decreased interactions with Cdc24p. The isolation of one mutation (V44A) correlated with
the observations that the T35A effector domain mutation could interfere with Cdc42 D118A,C188S p-Cdc24p interactions and could suppress the cdc42
D118A mutation, suggesting that Cdc24p may interact with Cdc42p through its effector domain. The cdc42
G12V mutant phenotypes were suppressed by the intragenic T35A and K183â187Q mutations and in skm1 Î and cla4 Î cells but not ste20 Î cells, suggesting that the mechanism of cdc42
G12V action is through the Skm1p and Cla4p protein kinases at the plasma membrane. Two intragenic suppressors of cdc42
G12V were also identified that displayed a dominant negative phenotype at 16â°C, which was not suppressed by overexpression of
Cdc24p, suggesting an alternate mechanism of action for these dominant negative mutations.
The responses of vascular endothelial cells (EC) to tumor necrosis factor-alpha (TNF), interleukin-1alpha (IL-1), and phorbol myristate acetate (PMA) were compared with respect to the kinetics of (i) ...NF-kappaB activation, (ii) IkappaB-alpha and IkappaB-beta degradation, and (iii) NF-kappaB-dependent cell surface molecule expression. TNF rapidly (</=20 min) and persistently (>20 h) activates NF-kappaB; IL-1 rapidly activates NF-kappaB, but activity declines by 3 h and further by 20 h; PMA slowly and transiently activates NF-kappaB. Untreated EC contain the inhibitory proteins IkappaB-alpha and IkappaB-beta. The onset of NF-kappaB activation correlates with degradation of IkappaB-alpha, but IkappaB-alpha reappears by 4 h without resequestration of NF-kappaB. TNF causes a rapid but partial (50%) reduction in IkappaB-beta, which does not recover by 22 h; IL-1 and PMA cause slower and less sustained reductions in IkappaB-beta. All three agonists induce de novo expression of E-selectin (CD62E) and vascular cell adhesion molecule-1 (CD106) and increase expression of intercellular adhesion molecule-1 (CD54) at 4 h. TNF induces sustained increases in vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 and increases human leukocyte antigen class I molecules at 24 h. We conclude that TNF causes persistent activation of NF-kappaB in human EC and that this may result from sustained reductions in IkappaB-beta levels.
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