bluuebunny/crossref_metadata_2025 huggingface dataset:
Genetic Variation of the Bloom-Forming CyanobacteriumMicrocystis aeruginosawithin and among Lakes: Implications for Harmful Algal Blooms
Authors: Wilson Alan E. , Sarnelle Orlando , Neilan Brett A. , Salmon Tim P. , Gehringer Michelle M. , Hay Mark E.
Published: October 2005

To measure genetic variation within and among populations of the bloom-forming cyanobacteriumMicrocystis aeruginosa, we surveyed a suite of lakes in the southern peninsula of Michigan that vary in productivity (total phosphorus concentrations of ∼10 to 100 μg liter−1). Survival ofM. aeruginosaisolates from lakes was relatively low (i.e., mean of 7% and maximum of 30%) and positively related to lake total phosphorus concentration (P= 0.014,r2= 0.407,n= 14). In another study (D. F. Raikow, O. Sarnelle, A. E. Wilson, and S. K. Hamilton, Limnol. Oceanogr. 49:482-487, 2004), survival rates ofM. aeruginosaisolates collected from an oligotrophic lake (total phosphorus of ∼10 μg liter−1and dissolved inorganic nitrogen:total phosphorus ratio of 12.75) differed among five different medium types (Gtest,Pof <0.001), with higher survival (P= 0.003) in low-nutrient media (28 to 37% survival) than in high-nutrient media. Even with the relatively low isolate survivorship that could select against detecting the full range of genetic variation, populations ofM. aeruginosawere genetically diverse within and among lakes (by analysis of molecular variance, Φsc= 0.412 [Φscis an F-statistic derivative which evaluates the correlation of haplotypic diversity within populations relative to the haplotypic diversity among all sampled populations],P= 0.001), with most clones being distantly related to clones collected from lakes directly attached to Lake Michigan (a Laurentian Great Lake) and culture collection strains collected from Canada, Scotland, and South Africa. Ninety-one percent of the 53 genetically uniqueM. aeruginosaclones contained the microcystin toxin gene (mcyA). Genotypes with the toxin gene were found in all lakes, while four lakes harbored both genotypes possessing and genotypes lacking the toxin gene.
Survival or Growth of
Escherichia coli
O157:H7 in a Model System of Fresh Meat Decontamination Runoff Waste Fluids and Its Resistance to Subsequent Lactic Acid Stress
Authors: Samelis John , Sofos John N. , Kendall Patricia A. , Smith Gary C.
Published: October 2005

A potential may exist for survival of and resistance development by
Escherichia coli
O157:H7 in environmental niches of meat plants applying carcass decontamination interventions. This study evaluated (i) survival or growth of acid-adapted and nonadapted
E. coli
O157:H7 strain ATCC 43895 in acetic acid (pH 3.6 ± 0.1) or in water (pH 7.2 ± 0.2) fresh beef decontamination runoff fluids (washings) stored at 4, 10, 15, or 25°C and (ii) resistance of cells recovered from the washings after 2 or 7 days of storage to a subsequent lactic acid (pH 3.5) stress. Corresponding cultures in sterile saline or in heat-sterilized water washings were used as controls. In acetic acid washings, acid-adapted cultures survived better than nonadapted cultures, with survival being greatest at 4°C and lowest at 25°C. The pathogen survived without growth in water washings at 4 and 10°C, while it grew by 0.8 to 2.7 log cycles at 15 and 25°C, and more in the absence of natural flora.
E. coli
O157:H7 cells habituated without growth in water washings at 4 or 10°C were the most sensitive to pH 3.5, while cells grown in water washings at 15 or 25°C were relatively the most resistant, irrespective of previous acid adaptation. Resistance to pH 3.5 of
E. coli
O157:H7 cells habituated in acetic acid washings for 7 days increased in the order 15°C > 10°C > 4°C, while at 25°C cells died off. These results indicate that growth inhibition by storage at low temperatures may be more important than competition by natural flora in inducing acid sensitization of
E. coli
O157:H7 in fresh meat environments. At ambient temperatures in meat plants,
E. coli
O157:H7 may grow to restore acid resistance, unless acid interventions are applied to inhibit growth and minimize survival of the pathogen. Acid-habituated
E. coli
O157:H7 at 10 to 15°C may maintain a higher acid resistance than when acid habituated at 4°C. These responses should be evaluated with fresh meat and may be useful for the optimization of decontamination programs and postdecontamination conditions of meat handling.
Electrochemical Polarization-Induced Changes in the Growth of Individual Cells and Biofilms of
Pseudomonas fluorescens
(ATCC 17552)
Authors: Busalmen Juan Pablo , de Sánchez Susana R.
Published: October 2005

The effect of surface electrochemical polarization on the growth of cells of
Pseudomonas fluorescens
(ATCC 17552) on gold electrodes has been examined. Potentials positive or negative to the potential of zero charge (PZC) of gold were applied, and these resulted in changes in cell morphology, size at cell division, time to division, and biofilm structure. At −0.2 V (Ag/AgCl-3 M NaCl), cells elongated at a rate of up to 0.19 μm min
−1
, rendering daughter cells that reached up to 3.8 μm immediately after division. The doubling time for the entire population, estimated from the increment in the fraction of surface covered by bacteria, was 82 ± 7 min. Eight-hour-old biofilms at −0.2 V were composed of large cells distributed in expanded mushroom-like microcolonies that protruded several micrometers in the solution. A different behavior was observed under positive polarization. At an applied potential of 0.5 V, the doubling time of the population was 103 ± 8 min, cells elongated at a lower rate (up to 0.08 μm min
−1
), rendering shorter daughters (2.5 ± 0.5 μm) after division, although the duplication times were virtually the same at all potentials. Biofilms grown under this positive potential were composed of short cells distributed in a large number of compact microcolonies. These were flatter than those grown at −0.2 V or at the PZC and were pyramidal in shape. Polarization effects on cell growth and biofilm structure resembled those previously reported as produced by changes in the nutritional level of the culture medium.
Diversity and Distribution of Sulfate-Reducing Bacteria in Permanently Frozen Lake Fryxell, McMurdo Dry Valleys, Antarctica
Authors: Karr Elizabeth A. , Sattley W. Matthew , Rice Melissa R. , Jung Deborah O. , Madigan Michael T. , Achenbach Laurie A.
Published: October 2005

The permanently frozen freshwater Lake Fryxell, located in the Dry Valleys of Antarctica, exhibits an ideal geochemistry for microbial sulfate reduction. To investigate the population of sulfate-reducing bacteria in Lake Fryxell, both 16S rRNA gene and metabolic primer sets targeting thedsrAgene for the dissimilatory sulfite reductase alpha subunit were employed to analyze environmental DNA obtained from the water column and sediments of Lake Fryxell. In addition, enrichment cultures of sulfate-reducing bacteria established at 4°C from Lake Fryxell water were also screened using thedsrAprimer set. The sequence information obtained showed that a diverse group of sulfate-reducing prokaryotes of the domainBacteriainhabit Lake Fryxell. With one exception, the enrichment culture sequences were not represented within the environmental sequences. Sequence data were compared with the geochemical profile of Lake Fryxell to identify possible connections between the diversity of sulfate-reducing bacteria and limnological conditions. Several clone groups were highly localized with respect to lake depth and, therefore, experienced specific physiochemical conditions. However, all sulfate-reducing bacteria inhabiting Lake Fryxell must function under the constantly cold conditions characteristic of this extreme environment.
Deletion of the
sigB
Gene in
Bacillus cereus
ATCC 14579 Leads to Hydrogen Peroxide Hyperresistance
Authors: van Schaik Willem , Zwietering Marcel H. , de Vos Willem M. , Abee Tjakko
Published: October 2005

The
sigB
gene of
Bacillus cereus
ATCC 14579 encodes the alternative sigma factor σ
B
. Deletion of
sigB
in
B. cereus
leads to hyperresistance to hydrogen peroxide. The expression of
katA
, which encodes one of the catalases of
B. cereus
, is upregulated in the
sigB
deletion mutant, and this may contribute to the hydrogen peroxide-resistant phenotype.
Analysis of Methane Monooxygenase Genes in Mono Lake Suggests That Increased Methane Oxidation Activity May Correlate with a Change in Methanotroph Community Structure
Authors: Lin Ju-Ling , Joye Samantha B. , Scholten Johannes C. M. , Schäfer Hendrik , McDonald Ian R. , Murrell J. Colin
Published: October 2005

Mono Lake is an alkaline hypersaline lake that supports high methane oxidation rates. Retrieved
pmoA
sequences showed a broad diversity of aerobic methane oxidizers including the type I methanotrophs
Methylobacter
(the dominant genus),
Methylomicrobium
, and
Methylothermus
, and the type II methanotroph
Methylocystis
. Stratification of Mono Lake resulted in variation of aerobic methane oxidation rates with depth. Methanotroph diversity as determined by analysis of
pmoA
using new denaturing gradient gel electrophoresis primers suggested that variations in methane oxidation activity may correlate with changes in methanotroph community composition.
PHOTOLUMINESCENCE OF ULTRA SMALL InAs/GaAs QUANTUM DOTS
Authors: LIN Y. G. , WU C. H. , TYAN S. L. , LIN S. D. , LEE C. P.
Published: October 2005

The InAs/GaAs quantum dots (QDs) with a baselength of less than 10 nm are studied by the excitation-, temperature-dependent and magneto-photoluminescence (PL). The baselengths of the QDs, calculated by the PL ground state transition energy and estimated by magneto-PL spectra, are in agreement with the result of atomic force microscopy measurements. By means of the excitation-dependent PL, we demonstrate that only the ground electron and hole states exist when the baselength of the QDs is smaller than about 7.3 nm, whereas the larger dots with a baselength of about 8.7 nm will give rise to one excited hole state. The measured energy separation between the ground and the excited hole states is in good agreement with the theoretical calculation. The transition energy in temperature-dependent PL spectra shows a rapid redshift as the temperature is higher than the critical temperature. The redshift rate is about 2.8 and 2.5 times larger than the values calculated by Varshni's law for small and large dots respectively. The higher redshift rate can be explained by the stronger tunneling effect. In addition, the PL linewidths show a V-shape dependence with the temperature. This behavior could be well described as a tunneling and electron-phonon scattering effect.
A TREATMENT OF THE QUANTUM PARTIAL ENTROPIES IN THE ATOM-FIELD INTERACTION WITH A CLASS OF SCHRÖDINGER CAT STATES
Authors: OBADA A.-S. F. , HESSIAN H. A. , ABDEL-ATY MAHMOUD
Published: October 2005

This paper is an enquiry into the circumstances under which entropy and subentropy methods can give an answer to the question of quantum entanglement in the composite state. Using a general quantum dynamical system, we obtain the analytical solution when the atom initially starts from its excited state and the field in different initial states. Different features of the entanglement are investigated when the field is initially assumed to be in a coherent state, an even coherent state (Schrödinger cate state), and a statistical mixture of coherent states. Our results show that the setting of the initial state and the Stark shift play important roles in the evolution of the sub-entropies and entanglement.
REMOTE STATE PREPARATION OF QUANTUM STATES VIA CAVITY QED
Authors: YE LIU , MA YUN-CHAO , GUO GUANG-CAN
Published: October 2005

In this paper, we give an experimentally feasible scheme for the remote state preparation by the prior share of an entangled state in cavity QED. The whole process of the remote state preparation for a single-atom state and a two-atom entangled state is shown. We find that only one classical bit and one single-atom state measurement is needed for the remote state preparation of a multi-atom entangled state.
ENTANGLEMENT IN THE XY SPIN CHAIN WITH NONUNIFORM EXTERNAL MAGNETIC FIELDS
Authors: CAO JUNPENG , SUN Z. Z. , SUN YIN , WANG YUPENG , WANG X. R.
Published: October 2005

We study the entanglement in the three-site Heisenberg XY model with nonuniform external magnetic fields and obtain analytic expressions for the measures of entanglement in the system with both the periodic and the open boundary conditions. We show that both the ground state and the excited states of the system possess remarkable entanglement properties and the entanglement clearly depends on the magnitude of external fields. We obtain the pairwise thermal entanglement of the system. We also discuss the boundary effects on the entanglement.
Cardioprotection afforded by NF-κB ablation is associated with activation of Akt in mice overexpressing TNF-α
Authors: Higuchi Yoshihiro , Chan Tung O. , Brown Maria A. , Zhang Jin , DeGeorge Brent R. , Funakoshi Hajime , Gibson Gregory , McTiernan Charles F. , Kubota Toru , Jones W. Keith , Feldman Arthur M.
Published: October 2005

When selectively overexpressed in mouse heart, TNF-α effects the development of a cardiomyopathy that closely mimics that seen in human failing hearts. It has been suggested that two intracellular signaling pathways, the Akt protein kinase and the NF-κB transcription factor, mediated TNF-α signaling. The present experiments assessed the effects of TNF-α overexpression on these two target proteins in vivo. We measured cardiac Akt kinase phosphorylation and NF-κB activity in mice overexpressing TNF-α (TNF1.6). Both basal and insulin-stimulated Akt phosphorylation were reduced by almost 70% by TNF-α overexpression. By contrast, NF-κB was robustly activated. These effects were absent when TNF-α receptor 1 (TNFR1) was selectively ablated. Cardiomyocyte-specific overexpression of the dominant-negative inhibitory κB protein transgene and subsequent inhibition of NF-κB activity attenuated the effects of TNF-α on Akt phosphorylation. NF-κB inhibition also significantly improved fractional shortening and diminished ventricular hypertrophy and survival without affecting infiltrative inflammation or cytokine expression. Thus, while overexpression of TNF-α effected a marked Akt inhibition and NF-κB activation in mouse hearts, inhibition of NF-κB offered salutary benefits mediated at least in part through activation of Akt.
Interactions of plasma osmolality with arterial and central venous pressures in control of sympathetic activity and heart rate in humans
Authors: Charkoudian N. , Eisenach J. H. , Joyner M. J. , Roberts S. K. , Wick D. E.
Published: October 2005

Plasma osmolality alters control of sympathetic activity and heart rate in animal models; however, it is unknown whether physiological increases in plasma osmolality have such influences in humans and what effect concurrent changes in central venous and/or arterial pressures may have. We tested whether physiological increases in plasma osmolality (similar to those during exercise dehydration) alter control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in humans. We studied 17 healthy young adults (7 women, 10 men) at baseline and during arterial pressure (AP) transients induced by sequential injections of nitroprusside and phenylephrine, under three conditions: control (C), after 1 ml/kg intravenous hypertonic saline (HT1), and after 2 ml/kg hypertonic saline (HT2). We continuously measured HR, AP, central venous pressure (CVP; peripherally inserted central catheter) and MSNA (peroneal microneurography) in all conditions. Plasma osmolality increased from 287 ± 1 mosmol/kg in C to 290 ± 1 mosmol/kg in HT1 ( P < 0.05) but did not increase further in HT2 (291 ± 1 mosmol/kg; P > 0.05 vs. C). Mean AP and CVP were similar between C and HT1, but both increased slightly in HT2. HR increased slightly but significantly during both HT1 and HT2 vs. C ( P < 0.05). Sensitivity of baroreflex control of MSNA was significantly increased vs. C in HT1 [−7.59 ± 0.97 (HT1) vs. −5.85 ± 0.63 (C) arbitrary units (au)·beat−1·mmHg−1; P < 0.01] but was not different in HT2 (−6.55 ± 0.94 au·beat−1·mmHg−1). We conclude that physiological changes in plasma osmolality significantly alter control of MSNA and HR in humans, and that this influence can be modified by CVP and AP.
Activated platelets contribute importantly to myocardial reperfusion injury
Authors: Xu Yaqin , Huo Yuqing , Toufektsian Marie-Claire , Ramos Susan I. , Ma Yongguang , Tejani Ankit D. , French Brent A. , Yang Zequan
Published: October 2005

Platelets become activated during myocardial infarction (MI), but the direct contribution of activated platelets to myocardial reperfusion injury in vivo has yet to be reported. We tested the hypothesis that activated platelets contribute importantly to reperfusion injury during MI in mice. After 30 min of ischemia and 60 min of reperfusion, P-selectin knockout mice had a significantly smaller infarct size than that of wild-type mice ( P < 0.05). Platelets were detected by P-selectin antibody in the previously ischemic region of wild-type mice as early as 2 min postreperfusion after 45 min, but not 20 min, of ischemia. The appearance of neutrophils in the heart was delayed when compared with platelets. Flow cytometry showed that the number of activated platelets more than doubled after 45 min of ischemia when compared with 20 min of ischemia or sham treatment ( P < 0.05). Platelet-rich or platelet-poor plasma was then transfused from either sham-operated or infarcted mice after 45 and 10 min of ischemia-reperfusion to mice undergoing 20 and 60 min of ischemia-reperfusion. Infarct size was increased by threefold and platelet accumulation was remarkably enhanced in mice treated with wild-type, MI-activated platelet-rich plasma but not in mice receiving either platelet-poor plasma from wild types or MI-activated platelet-rich plasma from P-selectin knockout mice. In conclusion, circulating platelets become activated early during reperfusion and their activation depends on the duration of the preceding coronary occlusion and is proportional to the extent of myocardial injury. Activated platelets play an important role in the process of myocardial ischemia-reperfusion injury, and platelet-derived P-selectin is a critical mediator.
Role of calmodulin methionine residues in mediating productive association with cardiac ryanodine receptors
Authors: Balog Edward M. , Norton Laura E. , Thomas David D. , Fruen Bradley R.
Published: October 2005

Calmodulin (CaM) binds to the cardiac ryanodine receptor Ca2+release channel (RyR2) with high affinity and may act as a regulatory channel subunit. Here we determine the role of CaM Met residues in the productive association of CaM with RyR2, as assessed via determinations of [3H]ryanodine and [35S]CaM binding to cardiac muscle sarcoplasmic reticulum (SR) vesicles. Oxidation of all nine CaM Met residues abolished the productive association of CaM with RyR2. Substitution of the COOH-terminal Mets of CaM with Leu decreased the extent of CaM inhibition of cardiac SR (CSR) vesicle [3H]ryanodine binding. In contrast, replacing the NH2-terminal Met of CaM with Leu increased the concentration of CaM required to inhibit CSR [3H]ryanodine binding but did not alter the extent of inhibition. Site-specific substitution of individual CaM Met residues with Gln demonstrated that Met124 was required for both high-affinity CaM binding to RyR2 and for maximal CaM inhibition. These results thus identify a Met residue critical for the productive association of CaM with RyR2 channels.
Alterations in blood-brain barrier ICAM-1 expression and brain microglial activation after λ-carrageenan-induced inflammatory pain
Authors: Huber J. D. , Campos C. R. , Mark K. S. , Davis T. P.
Published: October 2005

Previous studies showed that peripheral inflammatory pain increased blood-brain barrier (BBB) permeability and altered tight junction protein expression and the delivery of opioid analgesics to the brain. What remains unknown is which pathways and mediators during peripheral inflammation affect BBB function and structure. The current study investigated effects of λ-carrageenan-induced inflammatory pain (CIP) on BBB expression of ICAM-1. We also examined the systemic contribution of a number of proinflammatory cytokines and microglial activation in the brain to elucidate pathways involved in BBB disruption during CIP. We investigated ICAM-1 RNA and protein expression levels in isolated rat brain microvessels after CIP using RT-PCR and Western blot analyses, screened inflammatory cytokines during the time course of inflammation, assessed white blood cell counts, and probed for BBB and central nervous system stimulation and leukocyte transmigration using immunohistochemistry and flow cytometry. Results showed an early increase in ICAM-1 RNA and protein expression after CIP with no change in circulating levels of several proinflammatory cytokines. Changes in ICAM-1 protein expression were noted at 48 h. Immunohistochemistry showed that the induction of ICAM-1 was region specific with increased expression noted in the thalamus and frontal and parietal cortices, which directly correlated with increased expression of activated microglia. The findings of the present study were that CIP induces increased ICAM-1 mRNA and protein expression at the BBB and that systemic proinflammatory mediators play no apparent role in the early response (1–6 h); however, brain region-specific increases in microglial activation suggest a potential for a central-mediated response.
Increased blood flow causes coordinated upregulation of arterial eNOS and biosynthesis of tetrahydrobiopterin
Authors: Lam Chen-Fuh , Peterson Timothy E. , Richardson Darcy M. , Croatt Anthony J. , d'Uscio Livius V. , Nath Karl A. , Katusic Zvonimir S.
Published: October 2005

Shear stress, imposed on the vascular endothelium by circulating blood, critically sustains vascular synthesis of nitric oxide (NO). Endothelial NO synthase (eNOS) activity is determined by heat shock protein 90 (HSP90), caveolin-1, and the cofactor tetrahydrobiopterin (BH4). To determine whether increased blood flow concomitantly upregulates eNOS and GTP cyclohydrolase I (GTPCH I, the rate-limiting enzyme in BH4biosynthesis), an aortocaval fistula model in the rat was employed wherein aortic blood flow is enhanced proximal but decreased distal to the fistula. Eight weeks after the creation of the aortocaval fistula, the proximal and distal aortic segments were harvested; sham-operated rats served as controls. Vasomotor function was assessed by isometric force recording. Expression of eNOS, HSP90, caveolin-1, Akt, phosphorylated eNOS (eNOS-Ser1177), and GTPCH I were determined by Western blot analysis. Biosynthesis of BH4and GTPCH-I activity was examined by HPLC. In the aortic segments exposed to increased flow, contractions to KCl and phenylephrine were reduced, whereas endothelium-dependent relaxations were not affected compared with sham-operated or aortic segments with reduced blood flow. Expression of eNOS, caveolin-1, phosphorylated Akt, and eNOS-Ser1177 was enhanced in aortas exposed to increased blood flow. High flow augmented levels of cGMP and BH4and increased expression of GTPCH I. In aggregate, these findings provide the first demonstration in vivo that coordinated vascular upregulation of eNOS, and GTPCH I accompanies increased blood flow. This induction of GTPCH I increases BH4production, thereby optimizing the generation of NO by eNOS and thus the adaptive, vasorelaxant response required in sustaining increased blood flow.
Abnormal mitochondrial bioenergetics and heart rate dysfunction in mice lacking very-long-chain acyl-CoA dehydrogenase
Authors: Exil Vernat J. , Gardner Carla D. , Rottman Jeffrey N. , Sims Harold , Bartelds Beatrijs , Khuchua Zaza , Sindhal Rekha , Ni Gemin , Strauss Arnold W.
Published: October 2005

Mitochondrial very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is associated with severe hypoglycemia, cardiac dysfunction, and sudden death in neonates and children. Sudden death is common, but the underlying mechanisms are not fully understood. We report on a mouse model of VLCAD deficiency with a phenotype induced by the stresses of fasting and cold, which includes hypoglycemia, hypothermia, and severe bradycardia. The administration of glucose did not rescue the mice under stress conditions, but rewarming alone consistently led to heart rate recovery. Brown adipose tissue (BAT) from the VLCAD−/−mice showed elevated levels of the uncoupling protein isoforms and peroxisome proliferator-activated receptor-α. Biochemical assessment of the VLCAD−/−mice BAT showed increased oxygen consumption, attributed to uncoupled respiration in the absence of stress. ADP-stimulated respiration was 23.05 (SD 4.17) and 68.24 (SD 6.3) nmol O2·min−1·mg mitochondrial protein−1for VLCAD+/+and VLCAD−/−mice, respectively ( P < 0.001), and carbonyl cyanide p-trifluoromethoxyphenylhydrazone-stimulated respiration was 35.9 (SD 3.6) and 49.3 (SD 9) nmol O2·min−1·mg mitochondrial protein−1for VLCAD+/+and VLCAD−/−mice, respectively ( P < 0.20), but these rates were insufficient to protect them in the cold. We conclude that disturbed mitochondrial bioenergetics in BAT is a critical contributing factor for the cold sensitivity in VLCAD deficiency. Our observations provide insights into the possible mechanisms of stress-induced death in human newborns with abnormal fat metabolism and elucidate targeting of specific substrates for particular metabolic needs.
Chronic angiotensin II AT1 receptor blockade increases cerebral cortical microvessel density
Authors: Munzenmaier Diane H. , Greene Andrew S.
Published: October 2005

Angiotensin II is known to stimulate angiogenesis in the peripheral circulation through activation of the angiotensin II type 1 (AT1) receptor. This study investigated the effect of angiotensin receptor blockade on cerebral cortical microvessel density. Rats (6–7 wk old, n = 5–17) were instrumented with femoral arterial and venous indwelling catheters for arterial blood pressure measurement and drug administration. Rats were treated for 3 or 14 days with the AT1 receptor blocker losartan (50 mg/day in drinking water) or vehicle. Brains were sectioned and immunostained for CD31, and microvessel density was measured. Treatment with losartan for 3 or 14 days resulted in a slight decrease in mean arterial blood pressure (3 days, 92 ± 1 mmHg; and 14 days, 99 ± 2 mmHg) compared with vehicle (109 ± 3 and 125 ± 4 mmHg, respectively). A furosemide + captopril 14-day treatment group was added to control for the blood pressure change (96 ± 3 mmHg). Microvessel density increased in groups treated with losartan for 14 days (429 ± 13 vessels/mm2) compared with vehicle (383 ± 11 vessels/mm2) but did not change with furosemide + captopril (364 ± 7 vessels/mm2). Thus AT1 receptor blockade for 14 days resulted in increased cerebral microvessel density in a blood pressure-independent manner.
Human airway trypsin-like protease stimulates human bronchial fibroblast proliferation in a protease-activated receptor-2-dependent pathway
Authors: Matsushima Rie , Takahashi Akira , Nakaya Yutaka , Maezawa Hiroshi , Miki Mari , Nakamura Yoichi , Ohgushi Fumitaka , Yasuoka Susumu
Published: October 2005

Human airway trypsin-like protease (HAT) was isolated from airway secretions and localized to bronchial epithelial cells by immunohistochemistry. In the present study, we examined whether HAT could stimulate DNA synthesis and proliferation of primary human bronchial fibroblasts (HBF). HAT significantly stimulated the proliferation of HBF by 20–55%, a level similar to that of the mitogenic activity of lung mast cell tryptase (MCT). HAT also stimulated the incorporation of [3H]thymidine in HBF, and this HAT-induced DNA synthesis was abolished by leupeptin. Protease-activated receptor-2 (PAR-2) mRNA was expressed and localized to the cell surface in HBF. PAR-2 activating peptide (AP) also enhanced DNA synthesis, and both HAT and PAR-2 AP induced receptor internalization, similar to the response to trypsin. Pretreatment of HBF with anti-PAR-2 antibody significantly suppressed both HAT and PAR-2 AP-induced DNA synthesis. In addition, HAT and PAR-2 AP induced intracellular Ca2+mobilization in HBF. The HAT-induced increase in Ca2+was desensitized by pretreatment with trypsin or PAR-2 AP. U0126, a specific MAPK inhibitor, completely inhibited HAT-induced DNA synthesis as well as HAT-induced phosphorylation of MAPK. The effect of HAT and MCT together was additive, whereas the effect of HAT and insulin together on HBF DNA synthesis was synergistic. These results indicate that HAT stimulates fibroblast proliferation in bronchial airways through a PAR-2-dependent MEK-MAPK mediated pathway and that HAT is linked to airway processes involving fibroblasts.
Surfactant protein D enhancesPneumocystisinfection in immune-suppressed mice
Authors: Vuk-Pavlović Zvezdana , Mo Eun K. , Icenhour Crystal R. , Standing Joseph E. , Fisher James H. , Limper Andrew H.
Published: October 2005

To further determine the role of surfactant protein (SP)-D in the pathogenesis of Pneumocystis pneumonia, a mouse model of transgenic overexpression (OE) of SP-D was studied. These animals produce roughly 30- to 50-fold greater SP-D than their wild-type (WT) counterparts but show no other differences in lung morphology and function. Animals in both the SP-D OE and WT groups were depleted of CD4 lymphocytes with weekly injections of GK1.5 antibody, before Pneumocystis inoculation, and throughout the subsequent infection period. At various time points, mice were killed and analyzed for inflammatory parameters and organism burden. Proinflammatory cytokines in bronchoalveolar lavage fluid were elevated throughout the period of infection, with OE animals exhibiting significantly higher levels of TNF-α and macrophage inflammatory protein-2 compared with WT controls. The total number of cells in the lavage fluid was also increased significantly only in the OE group, whereas the cell differential composition demonstrated lymphocyte and eosinophil infiltration in both groups of animals. Significantly, the organism burden was markedly higher in the SP-D OE animals, whereas the WT mice demonstrated little alteration in organism number over the course of infection. These results further indicate that SP-D facilitates the development of Pneumocystis infection and related lung inflammation in an immunosuppressed mouse model.
Role of 12-lipoxygenase in hypoxia-induced rat pulmonary artery smooth muscle cell proliferation
Authors: Preston Ioana R. , Hill Nicholas S. , Warburton Rod R. , Fanburg Barry L.
Published: October 2005

The 12-lipoxygenase (12-LO) pathway of arachidonic acid metabolism stimulates cell growth and metastasis of various cancer cells and the 12-LO metabolite, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], enhances proliferation of aortic smooth muscle cells (SMCs). However, pulmonary vascular effects of 12-LO have not been previously studied. We sought evidence for a role of 12-LO and 12(S)-HETE in the development of hypoxia-induced pulmonary hypertension. We found that 12-LO gene and protein expression is elevated in lung homogenates of rats exposed to chronic hypoxia. Immunohistochemical staining with a 12-LO antibody revealed intense staining in endothelial cells of large pulmonary arteries, SMCs (and possibly endothelial cells) of medium and small-size pulmonary arteries and in alveolar walls of hypoxic lungs. 12-LO protein expression was increased in hypoxic cultured rat pulmonary artery SMCs. 12(S)-HETE at concentrations as low as 10−5μM stimulated proliferation of pulmonary artery SMCs. 12(S)-HETE induced ERK 1/ERK 2 phosphorylation but had no effect on p38 kinase expression as assessed by Western blotting. 12(S)-HETE-stimulated SMC proliferation was blocked by the MEK inhibitor PD-98059, but not by the p38 MAPK inhibitor SB-202190. Hypoxia (3%)-stimulated pulmonary artery SMC proliferation was blocked by both U0126, a MEK inhibitor, and baicalein, an inhibitor of 12-LO. We conclude that 12-LO and its product, 12(S)-HETE, are important intermediates in hypoxia-induced pulmonary artery SMC proliferation and may participate in hypoxia-induced pulmonary hypertension.
Lysophosphatidic acid enhances interleukin-13 gene expression and promoter activity in T cells
Authors: Rubenfeld Joshua , Guo Jia , Sookrung Nitat , Chen Rongbing , Chaicumpa Wanpen , Casolaro Vincenzo , Zhao Yutong , Natarajan Viswanathan , Georas Steve
Published: October 2005

Lysophosphatidic acid (LPA) is a membrane-derived lysophospholipid with wide-ranging effects on multiple lung cells including airway epithelial and smooth muscle cells. LPA can augment migration and cytokine synthesis in lymphocytes, but its potential effects on Th2 cytokines have not been well studied. We examined the effects of physiological concentrations of LPA on IL-13 gene expression in human T cells. The Jurkat T cell line and human peripheral blood CD4+ T cells were incubated with LPA alone or with 1) pharmacological agonists of different signaling pathways, or 2) antibodies directed against the T cell receptor complex and costimulatory molecules. Luciferase-based reporter constructs driven by different lengths of the human IL-13 promoter were transfected by electroporation in Jurkat cells treated with and without LPA. The effects of LPA on IL-13 mRNA stability were examined using actinomycin D to halt ongoing transcription. Expression of mRNA encoding LPA2and LPP-1 increased with T cell activation. LPA augmented IL-13 secretion under conditions of submaximal T cell activation. This was observed using pharmacological agonists activating intracellular calcium-, PKC-, and cAMP-dependent signaling pathways, as well as antibodies directed against CD3 and CD28. LPA only slightly prolonged IL-13 mRNA half-life in submaximally stimulated Jurkat cells. In contrast, LPA significantly enhanced transcriptional activation of the IL-13 promoter via regulatory elements contained within proximal 312 bp. The effects of LPA on IL-13 promoter activation appeared to be distinct from those mediated by GATA-3. LPA can augment IL-13 gene expression in T cells, especially under conditions of submaximal activation.
Optimal boundary control of distributed systems involving dynamic boundary conditions
Authors: Kerbal S. , Ahmed N. U.
Published: October 2005

In this paper we consider Lagrange type control problem for systems involving dynamic boundary conditions that is, with boundary operators containing time derivatives. Assuming the existence of optimal controls, B‐evolutions theory is used to present necessary conditions of optimality. The result is illustrated by an example from heat transfer problem and also an algorithm for computing optimal controls is presented.
The V‐transform: A tool for analysis of control systems robustness with respect to disturbance model uncertainty
Authors: Davison D. E. , Kabamba P. T. , Meerkov S. M.
Published: October 2005

This work is motivated by the need forr tools for the analysis of disturbance model uncertainty in feedback control systems. Such tools are developed in this paper for the case where the disturbance is modeled as the output of a first‐order filter which is driven by white noise and whose bandwidth, ωd, and gain, K, are uncertain. An analytical expression for the steady‐state output variance as a function of ωd
is derived: This function is referred to as a V‐transform, and is denoted by V(G)(ωd)
, where G(s) is the closed‐loop transfer function from disturbance to output. Properties of V‐transforms are investigated and the notions of disturbance gain margin and disturbance bandwidth margin, both measures of robustness with respect to disturbance model uncertainty, are introduced. Using these new tools, it is shown that there is a fundamental robustness performance limitation if the plant has nonminimum‐phase zeros, but no such limitation in the minimum‐phase case.
Decreased Contractile and Metabolic Reserve in Peroxisome Proliferator–Activated Receptor-α–Null Hearts Can Be Rescued by Increasing Glucose Transport and Utilization
Authors: Luptak Ivan , Balschi James A. , Xing Yanqiu , Leone Teresa C. , Kelly Daniel P. , Tian Rong
Published: October 2005

Background—

Downregulation of peroxisome proliferator–activated receptor-α (PPARα) in hypertrophied and failing hearts leads to the reappearance of the fetal metabolic pattern, ie, decreased fatty acid oxidation and increased reliance on carbohydrates. Here, we sought to elucidate the functional significance of this shift in substrate preference.

Methods and Results—

We assessed contractile function and substrate utilization using
13
C nuclear magnetic resonance spectroscopy and high-energy phosphate metabolism using
31
P nuclear magnetic resonance spectroscopy in perfused hearts isolated from genetically modified mice (PPARα
−/−
) that mimic the metabolic profile in myocardial hypertrophy. We found that the substrate switch from fatty acid to glucose (3-fold down) and lactate (3-fold up) in PPARα
−/−
hearts was sufficient for sustaining normal energy metabolism and contractile function at baseline but depleted the metabolic reserve for supporting high workload. Decreased ATP synthesis (measured by
31
P magnetization transfer) during high workload challenge resulted in progressive depletion of high-energy phosphate content and failure to sustain high contractile performance. Interestingly, the metabolic and functional defects in PPARα
−/−
hearts could be corrected by overexpressing the insulin-independent glucose transporter GLUT1, which increased the capacity for glucose utilization beyond the intrinsic response to PPARα deficiency.

Conclusions—

These findings demonstrate that metabolic remodeling in hearts deficient in PPARα increases the susceptibility to functional deterioration during hemodynamic overload. Moreover, our results suggest that normalization of myocardial energetics by further enhancing myocardial glucose utilization is an effective strategy for preventing the progression of cardiac dysfunction in hearts with impaired PPARα activity such as hearts with pathological hypertrophy.
Remodeling in Cells From Different Regions of the Reentrant Circuit During Ventricular Tachycardia
Authors: Baba Shigeo , Dun Wen , Cabo Candido , Boyden Penelope A.
Published: October 2005

Background—

Anisotropic reentrant excitation occurs in the remodeled substrate of the epicardial border zone (EBZ) of the 5-day infarcted canine heart. Reentry is stabilized because of the formation of functional lines of block. We hypothesized that regional differences of ionic currents in cells of the EBZ form these lines of block. Therefore, we first mapped reentrant circuits of sustained tachycardias, then dispersed cells (infarct zone cells, IZs) from the central common pathway of the circuit (IZc) as well as from the other side of the line of block (outer pathway, IZo) for study.

Methods and Results—

We mapped reentrant circuits in the EBZ of infarcted hearts during sustained ventricular tachycardias (>30 seconds, n=17 episodes, cycle lengths=218±7.9 ms).
I
Na
density was reduced in both IZc and IZo, and the kinetic properties of IZc
I
Na
were markedly altered versus IZo. Structural remodeling of the sodium channel protein Na
v
1.5 occurred in IZs, with cell surface localization differing from normal cells. Both IZc and IZo have similar but reduced
I
CaL
, whereas IZc showed changes in Ca
2+
current kinetics with an acceleration of current decay. Computer simulations of the 2D EBZ showed that incorporating only differences between
I
Na
in IZc and IZo prevented stability of the reentrant circuit. Incorporating only differences between
I
CaL
in the IZc and IZo cells also prevented stability of the circuit. However, incorporating both
I
Na
and
I
CaL
current differences stabilized the simulated reentrant circuit, and lines of block formed between the 2 distinct regions.

Conclusions—

Despite differences in
I
Na
and
I
CaL
properties in cells of the center and outer pathways of a reentrant circuit, the resulting changes in effective refractory periods tend to stabilize reentry in this remodeled substrate.
The genus Deficephalobus De Ley & Coomans, 1990 (Cephalobina: Osstellidae) from nature reserves in Costa Rica
Authors: Bongers Tom , Holovachov Oleksandr , Esquivel Alejandro
Published: October 2005

Two species of the genus Deficephalobus, D. mirabilis sp. n. and D. desenderi, are described and illustrated on the basis of material collected in Costa Rica. The new species is characterised by 0.67-1.2 mm long body; bluntly rounded labial region; amphidial aperture one-third of labial region diam. wide; cheilostom barrel-shaped with sclerotised, bar-shaped, cheilorhabdia; gymnostom barrel-shaped with moderately sclerotised lining of gymnostom; stegostom funnel-shaped anteriorly, narrow tubular posteriorly and subdivided into four sets of rhabdia; basal bulb elongate ovoid with weakly developed valvular apparatus; excretory pore opening anterior to nerve ring; ovary tip almost reaching the level of rectum, large spermatheca, postvulval uterine sac shorter than vulval body diameter; female tail elongate conoid and straight, with filiform tail terminus; male tail short conoid with small, ragged, terminal mucro.
Ecanema ecae gen. n., sp. n. (Nematoda: Dorylaimida) from Costa Rica
Authors: Shaheen Azra , Ahmad Wasim
Published: October 2005

Ecanema gen. n. is described from natural forest in Costa Rica. The new genus is characterised by having distinctly offset lip region, separate lips with distinctly projecting labial papillae, attenuated odontostyle, pharynx rather sac-like, apparently divisible into three regions, large S1N1, distinct cardiac glands, amphidelphic female genital system, short conoid tail and supplements beginning within the range of spicules in males. The type and only species, E. ecae sp. n., is characterised by having 0.87-0.98 mm long body; 19.5-20.5 μm long odontostyle; expanded part of pharynx comprising 36-41% of total neck length; pars refringens vaginae sclerotised and about one anal body diam. long, and conoid tail with acute terminus.
Assessment of inoculation methods in evaluating response of yam cultivars to infection by Scutellonema bradys
Authors: Baimey Hugues , Coyne Danny , Labuschagne Nico
Published: October 2005

Two glasshouse experiments were conducted to assess the influence of three inoculation methods on Scutellonema bradys multiplication on yam (Dioscorea spp.) and on growth and production of the crop. Three separate cultivars of yam were used in the study: two Dioscorea rotundata cultivars (Ala and Kpouna) and one Dioscorea cayenensis (Tabane). One-month-old plants were each inoculated with approximately 1000 S. bradys juveniles and adults. The inoculation methods included inoculation with chopped infected pieces of yam peel (about 0.5 × 0.3 cm2), chopped and blended infected yam peel and a water suspension (200 ml) of extracted nematodes compared with a S. bradys-free yam tuber peel control. The two experiments were harvested at 9 and 4 months after planting. Nematode population densities at harvest were significantly different (P ≤ 0.05) among inoculation methods and among yam cultivars. Higher nematode population densities were recorded on tubers from plants inoculated with unblended peel, followed by those inoculated with blended peel. Inoculation with nematode suspensions yielded the lowest nematode population densities. Inoculation with S. bradys did not affect the vine circumference and the number of tubers. Weights of tubers differed among inoculation methods for two of the three yam cultivars tested (P ≤ 0.05).
Increased penetration of host roots by nematodes after recovery from quiescence induced by root cap exudate
Authors: Hawes Martha , Stock S. Patricia , Flores-Lara Yolanda , Hubbard Jennifer , Schmitt Mark , McClure Michael
Published: October 2005

Fourteen of 20 plant species surveyed produced root cap exudates that induced a state of reversible quiescence in Meloidogyne incognita and Caenorhabditis elegans. Exudate from six species failed to induce quiescence in either nematode species. Root cap exudates from pea were found to trigger quiescence in populations of plant-parasitic, animal-parasitic, insect-pathogenic, and free-living nematode species. One animal parasite was resistant. Caenorhabditis elegans strains with defects in known metabolic pathways also were screened to explore the potential for using this model system to examine the genetic basis for exudates-induced quiescence (EIQ). All 62 lines tested exhibited wild type sensitivity to root cap exudates and preliminary efforts to obtain viable EIQ-resistant strains by ethyl methanesulphonate (EMS) mutagenesis were unsuccessful. After recovery from EIQ, penetration of alfalfa roots by second-stage juveniles of M. incognita more than doubled within 24 h, compared with controls, and the number of nematodes per root remained high for a week but long-term development and maturation was similar to that of untreated control inoculum. In cucumber, penetration after recovery from EIQ increased by several fold but returned to control levels within 4 days post-inoculation.
Variations in life history parameters and their influence on rate of population increase of different pathogenic isolates of the pine wood nematode, Bursaphelenchus xylophilus
Authors: Wang Yu , Suzuki Kazuo , Sakaue Daisuke , Yamada Toshihiro
Published: October 2005

Two virulent isolates and two avirulent isolates of Bursaphelenchus xylophilus and one isolate of B. mucronatus were used to investigate the relationships between life history parameters, rate of population increase and virulence. The results showed that on fungal cultures of Botrytis cinerea, virulent B. xylophilus completed one generation much faster than did avirulent B. xylophilus and B. mucronatus. There was a tendency that virulent B. xylophilus isolates laid more eggs during the egg laying period than did avirulent populations. Shorter generation time and higher fecundity resulted in a higher rate of population increase. Generation time and fecundity were primary factors determining rate of population increase. Difference in rate of population increase is closely related to variation of virulence: virulent B. xylophilus increased population size at the fastest rate, avirulent B. xylophilus was slower, and B. mucronatus was slowest. It is assumed that similar variations in life history parameters and rate of population increase are also expressed in pine trees and help to explain variation of virulence in the field.
Prey preference and feeding behaviour of the diplogastrid predator Mononchoides gaugleri (Nematoda: Diplogastrida)
Authors: Bilgrami Anwar , Gaugler Randy , Brey Christopher
Published: October 2005

Prey preference and feeding behaviour of Mononchoides gaugleri were studied using 11 phytoparasitic nematode species as prey. A full range of prey preferences were detected in no choice and paired choice predator-prey experiments. Meloidogyne incognita, Heterodera mothi and Anguina tritici juveniles (coefficient of preference = 0.92-1.00) were highly preferred as prey by M. gaugleri in all tests. The second tier of prey preference was occupied by the adult Hirschmanniella oryzae, Tylenchorhynchus mashhoodi, Xiphinema americanum and Paratrichodorus christiei (coefficient of preference = 0.19-0.67), and the third tier by Longidorus attenuatus and Helicotylenchus indicus (coefficient of preference = −0.15-−0.57). Hemicriconemoides mangiferae and Hoplolaimus indicus were not preyed upon. Mononchoides gaugleri attacked H. mothi and A. tritici (maximum strike rate (SR)= 92-94%), which has resulted in maximal prey wounding (encounters resulted in wounding (EW) = 46-47%). Longidorus attenuatus was attacked minimally (SR = 42%) with fewest casualties (EW = 21%). Hirschmanniella oryzae, H. mothi and M. incognita were most susceptible (prey susceptibility (PS) = 87.5-93.5%), whereas X. americanum and P. christiei were highly resistant prey species (prey resistance (PR) = 66.7-74.2%). Temperature and prey density governed predator feeding activities, with optimal search duration at 20-30°C and 150-225 prey. The shortest and longest feeding durations of Mononchoides gaugleri were recorded for M. incognita and L. attenuatus, respectively. Predation was density-dependent.