Fermilab Collider Run II: Accelerator Status and Upgrades

Fermilab will continue to maintain its pre-eminent position in the world of High Energy Physics, with a unique opportunity to make unprecedented studies of the top quark and major discoveries, until the Large Hadron collider (LHC) at CERN becomes operational near the end of the decade. Run II is well underway with major accelerator and detector upgrades since Run I. A program of further upgrades to the accelerator complex will result in an integrated luminosity of 4-8 fb-1 per experiment, by the year 2009.Comment: 12 pages, 6 figures. To be published in the Proceedings of the 15th Topical Conference on Hadron Collider Physics, HCP2004, Michigan State University, East Lansing, MI, June 14-18, 2004 (American Institute of Physics, NY, 2004

CO2 exchange characteristics during dark-light transitions in wild-type and mutant Chlamydomonas reinhardii cells

A burst of net CO2 uptake was observed during the first 3–4 min after the onset of illumination in both wild-type Chlamydomonas reinhardii in which carbonic anhydrase was chemically inhibited with ethoxyzolamide and in a mutant of C. reinhardii (ca-1-12-1C) deficient in carbonic anhydrase activity. The burst was followed by a rapid decrease in the CO2 uptake rate so that net evolution often occurred. After a 2–3 min period of CO2 evolution, net CO2 uptake again increased and ultimately reached a steady-state, positive rate. From [14CO2]-tracer studies it was determined that CO2 fixation proceeded at a nearly linear rate throughout the period of illumination. Thus, prior to reaching a steady state, there was a rapid accumulation of inorganic carbon inside the cells which apparently reached a supercritical concentration and the excess was excreted, causing a subsequent efflux of CO2. A post illumination burst of net CO2 efflux was also observed in ethoxyzolamide-inhibited wild type and ca-1 mutant cells, but not in the unihibited wild type. [14CO2]-tracer experiments revealed that this burst was the result of a collapse of a large internal inorganic carbon pool at the onset of darkness rather than a photorespiratory post-illumination burst. These results indicate that upon illumination, chemical or genetic inhibition of carbonic anhydrase initially causes an accumulation of excess inroganic carbon in C. reinhardii cells, and that unknown regulatory mechanisms correct for this imbalance by first excreting the excess inorganic carbon and then, after several dampened oscillations, achieving an equilibrium between bicarbonate uptake, bicarbonate dehydration, and CO2 fixation

Use of Mutants in Analysis of the CO2-Concentrating Pathway of Chlamydomonas Reinhardtii

In Chlamydomonas reinhardtii and other green algae, a pathway which actively concentrates CO2 at the site of ribulose 1,5-bisphosphate-carbozylase/oxygenase (RUBISCO) is responsible for the suppression of photo-respiration and oxygen inhibition of photosynthesis and for the stimulation of photosynthesis at a low external CO2 concentrations. Increased photosynthesis and reduced photorepiration in Chlamydomonas at air levels of CO2 and O2 are manifested by a high affinity for CO2 in photosynthesis, a nearly maximal photosynthetic rate, absence of O2 inhibition of CO2 fixation, low rates of synthesis of photo respiratory metabolites, and a near-zero CO2 compensation concentration (1,2). The CO2-concentrating pathway of Chlamydomonas is inducible, with induction occurring at air levels of CO2 but not at elevated (1-5%) concentrations of CO2 (2). Biochemical and physiological studies implicated the involvement of at least two components in the pathway, an energy-dependent, saturable inorganic transport process (1,9) and the enzyme carbonic anhydrase (CA) (1,2). Badger et al. (1) suggested that the role of CA in the pathway might be dehydration of transported HCO3 to supple CO2, the substrate of RUBISCO. In order to further characterize the Chlamydomonas CO2-concentrating pathway, we utilized existing, nonphotosynthetic mutants of C. rienhardtii fo study of induction requirements and set out to identify and characterize new mutant strains of C. reinhardtii with defects in the CO2-concentrating pathway itself. This work with Chlamydomonas mutants has helped firmly establish the requirement for photosynthetic competence in the induction of the pathway, unambiguously confirmed that at least two components, CA and HCO3 transport, are involved, and that the principal role of internal CA is dehydration of transported HCO3

Accessory cells in Murine Peyer’s patch: I. Identification and enrichment of a functional dendritic cell

[No abstract available

New frog

8 p. : ill., map ; 24 cm.Includes bibliographical references (p. 8)

Increased prevalence of the pfdhfr/phdhps quintuple mutant and rapid emergence of pfdhps resistance mutations at codons 581 and 613 in Kisumu, Kenya

<p>Abstract</p> <p>Background</p> <p>Anti-malarial drug resistance in Kenya prompted two drug policy changes within a decade: sulphadoxine-pyrimethamine (SP) replaced chloroquine (CQ) as the first-line anti-malarial in 1998 and artemether-lumefantrine (AL) replaced SP in 2004. Two cross-sectional studies were conducted to monitor changes in the prevalence of molecular markers of drug resistance over the period in which SP was used as the first-line anti-malarial. The baseline study was carried out from 1999-2000, shortly after implementation of SP, and the follow-up study occurred from 2003-2005, during the transition to AL.</p> <p>Materials and methods</p> <p>Blood was collected from malaria smear-positive, symptomatic patients presenting to outpatient centers in Kisumu, Kenya, during the baseline and follow-up studies. Isolates were genotyped at codons associated with SP and CQ resistance. <it>In vitro </it>IC₅₀values for antifolates and quinolones were determined for isolates from the follow-up study.</p> <p>Results</p> <p>The prevalence of isolates containing the <it>pfdhfr </it>N51I/C59R/S108N/<it>pfdhps </it>A437G/K540E quintuple mutant associated with SP-resistance rose from 21% in the baseline study to 53% in the follow-up study (p < 0.001). Isolates containing the <it>pfdhfr </it>I164L mutation were absent from both studies. The <it>pfdhps </it>mutations A581G and A613S/T were absent from the baseline study but were present in 85% and 61%, respectively, of isolates from the follow-up study. At follow-up, parasites with mutations at five <it>pfdhps </it>codons, 436, 437, 540, 581, and 613, accounted for 39% of isolates. The CQ resistance-associated mutations <it>pfcrt </it>K76T and <it>pfmdr1 </it>N86Y rose from 82% to 97% (p = 0.001) and 44% to 76% (p < 0.001), respectively, from baseline to follow-up.</p> <p>Conclusions</p> <p>During the period in which SP was the first-line anti-malarial in Kenya, highly SP-resistant parasites emerged, including isolates harboring <it>pfdhps </it>mutations not previously observed there. SP continues to be widely used in Kenya; however, given the highly resistant genotypes observed in this study, its use as a first-line anti-malarial should be discouraged, particularly for populations without acquired immunity to malaria. The increase in the <it>pfcrt </it>K76T prevalence, despite efforts to reduce CQ use, suggests that either these efforts are not adequate to alleviate CQ pressure in Kisumu, or that drug pressure is derived from another source, such as the second-line anti-malarial amodiaquine.</p

Historical ecology with real numbers: past and present extent and biomass of an imperiled estuarine habitat

Historic baselines are important in developing our understanding of ecosystems in the face of rapid global change. While a number of studies have sought to determine changes in extent of exploited habitats over historic timescales, few have quantified such changes prior to late twentieth century baselines. Here, we present, to our knowledge, the first ever large-scale quantitative assessment of the extent and biomass of marine habitat-forming species over a 100-year time frame. We examined records of wild native oyster abundance in the United States from a historic, yet already exploited, baseline between 1878 and 1935 (predominantly 1885–1915), and a current baseline between 1968 and 2010 (predominantly 2000–2010). We quantified the extent of oyster grounds in 39 estuaries historically and 51 estuaries from recent times. Data from 24 estuaries allowed comparison of historic to present extent and biomass. We found evidence for a 64 per cent decline in the spatial extent of oyster habitat and an 88 per cent decline in oyster biomass over time. The difference between these two numbers illustrates that current areal extent measures may be masking significant loss of habitat through degradation