bluuebunny/crossref_metadata_2025 huggingface dataset:
Coral reef quality and recreation fees in marine protected areas
Authors: Wielgus Jeffrey , Balmford Andrew , Lewis Tiffany B. , Mora Camilo , Gerber Leah R.
Published: November 2009

The recreational use of marine protected areas (MPAs) is a potential source of funding for MPAs in developing countries, for instance given the willingness of international divers to pay considerably higher diving fees than they currently pay. We conducted a global survey of MPAs containing coral reefs to investigate what factors are important in determining the size of fees charged to recreational SCUBA divers. The survey suggests that a negative perception about diving fees by managers is a more important predictor of fee size than the quality of diving, which can help explain the prevalently low size of diving fees. Decentralized fee systems and higher diving fees can help capture some of the surplus willingness to pay for diving in MPAs, but an excessive reliance on tourism for funding MPA management could expose coral reefs to damages.
Influence of dietary sodium on the blood pressure and renal sympathetic nerve activity responses to intracerebroventricular angiotensin II and angiotensin III in anaesthetized rats
Authors: Houghton Belinda L. , Huang Chunlong , Johns Edward J.
Published: October 2009

The regulation of blood pressure and sympathetic outflow by the brain renin–angiotensin system in animals subjected to raised or lowered dietary Na+intake is unclear. This study compared the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular (i.c.v.) infusion of angiotensin II (AngII) and III (AngIII) before and after peripheral V1receptor blockade (V1B) in α‐chloralose–urethane‐anaesthetized rats fed a low (0.03%, LNa+), normal (0.3%, NNa+) or high Na+diet (3.0%, HNa+) from 4 to 11 weeks of age. The rise in MAP 2 min post AngIIi.c.v. was greater in HNa+(14 ± 3 mmHg)versusLNa+(8 ± 1 mmHg,P< 0.05) and after AngIIIi.c.v. in HNa+(14 ± 3 mmHg)versusNNa+(6 ± 1 mmHg,P< 0.05) and LNa+(7 ± 1 mmHg,P< 0.05). The MAP responses to AngII and AngIIIi.c.v. were abolished after V1B in LNa+, but were only attenuated in HNa+. In NNa+, V1B blunted the MAP responses to AngII and abolished those to AngIII. The MAP remained elevated 30 min after AngII in all groups, but returned to baseline levels 15 min after AngIII in NNa+and HNa+(P< 0.01). Twenty minutes afteri.c.v. AngII, RSNA rose above baseline in HNa+(112 ± 1%), a response not observed in the LNa+and NNa+groups. Twenty minutes post AngIIIi.c.v., RSNA was elevated in both HNa (109 ± 2%) and NNa+(109 ± 2%). After V1B, RSNA rose only in the HNa+group 15 min post AngIII infusion (109 ± 1%). Together, these findings: (1) suggest that HNa+intake augments the MAP and RSNA responses toi.c.v. AngII and AngIII; (2) highlight an important role for peripheral V1receptors during these responses; and (3) differentiate the effects of AngII and AngIII on blood pressure and RSNA.
Vascular endothelial growth factor enhances cancer cell adhesion to microvascular endothelium in vivo
Authors: Shen Shang , Fan Jie , Cai Bin , Lv Yonggang , Zeng Min , Hao Yanyan , Giancotti Filippo G. , Fu Bingmei M.
Published: October 2009

To investigate whether vascular endothelial growth factor (VEGF) enhances cancer cell adhesion to normal microvessels, we used in vivo video microscopy to measure adhesion rates of MDA‐MB‐435s human breast cancer cells and ErbB2‐transformed mouse mammary carcinomas in the postcapillary venules of rat mesentery. An individual postcapillary venule in the mesentery was injected via a glass micropipette with cancer cells either in a perfusate of mammalian Ringer solution containing 1% bovine serum albumin as a control, or with the addition of 1 nm VEGF for test measurements. Cell adhesion was measured as either the number of adherent cells or the fluorescence intensity of adherent cells in a vessel segment for ∼60 min. Our results showed that during both control and VEGF treatments, the number of adherent cells increased almost linearly with time over 60 min. The VEGF treatment increased the adhesion rates of human tumour cells and mouse carcinomas 1.9‐fold and 1.8‐fold, respectively, over those in control conditions. We also measured cancer cell adhesion after pretreatment of cells with an antibody blocking VEGF or an antibody blocking α6 integrin, and pretreatment of the microvessel with VEGF receptor (KDR/Flk‐1) inhibitor, SU1498, or anti‐integrin extracellular matrix ligand antibody, anti‐laminin‐5. All antibodies and inhibitor significantly reduced adhesion, with anti‐VEGF and SU1498 reducing it the most. Our results indicate that VEGF enhances cancer cell adhesion to the normal microvessel wall, and further suggest that VEGF and its receptor, KDR/Flk‐1, as well as integrins of tumour cells and their ligands at the endothelium, contribute to mammary cancer cell adhesion to vascular endothelium in vivo.
Detraining losses of skeletal muscle capillarization are associated with vascular endothelial growth factor protein expression in rats
Authors: Malek Moh H. , Olfert I. Mark , Esposito Fabio
Published: October 2009

The purposes of this study were as follows: (1) to examine basal vascular endothelial growth factor (VEGF) protein concentrations following 10 weeks of endurance training and after 7 days of detraining; and (2) to examine the acute VEGF protein response to a single 1 h exercise work bout in trained and detrained animals in relationship to changes in capillary indices following training and detraining. Thirty‐three Sprague–Dawley rats were randomized into the following six groups: (1) control–basal; (2) control–acute exercise; (3) trained–basal; (4) trained–acute exercise; (5) detrained–basal; and (6) detrained–acute exercise. Groups 3–6 performed endurance training on a rodent treadmill three times per week for 10 weeks. Following the training intervention, rats in groups 5 and 6 remained cage confined (i.e. detrained) for 7 days. As expected, training increased soleus and plantaris muscle capillarity and attenuated the VEGF response to acute exercise. Seven days of detraining, however, resulted in a regression of capillary contacts and individual capillary‐to‐fibre ratio in the plantaris and soleus muscles compared with the trained group (P < 0.05). Restoration of the VEGF protein response to acute exercise was evident in both muscles, but only statistically significant in the plantaris muscle (P < 0.05). This is the first study to demonstrate the temporal relationship between VEGF protein expression and skeletal muscle capillarity within the first week of detraining. The findings of the present investigation are consistent with the hypothesis that reduced capillarity impairs oxygen availability to the working muscles. The results indicated that training‐induced angiogenic remodelling was reversible following 1 week of detraining and may be modulated by VEGF.
HBr based inductively coupled plasma etching of high aspect ratio nanoscale trenches in InP: Considerations for photonic applications
Authors: Sultana N. , Zhou Wei , LaFave Tim P. , MacFarlane Duncan L.
Published: October 2009

Pure HBr based inductively coupled plasma vertical, anisotropic etching provides high aspect ratio (20–40) nanoscale trenches in InP at 165°C processing temperatures. Since these temperatures are comparatively lower than chlorine based chemistries, HBr should yield improved device reliability. In addition to temperature dependence, other important considerations for integrated photonic applications are discussed. The phenomenon of aspect ratio dependent etching, or reactive ion etching lag, begins to manifest itself when the etch aspect ratio of InP approaches 30:1. No microloading effect is observed in the 100nm scale trench etching. Physical etch dominates the etching mechanism in this regime, and acceptably smooth, 20nm rms surface roughness is observed.
Measuring interface electrostatic potential and surface charge in a scanning electron microscope
Authors: Sychugov I. , Nakayama Y. , Mitsuishi K.
Published: October 2009

A novel method for electrostatic potential measurements at the interface is described. It involves placing a two-dimensional grid below the sample and observing it in a scanning electron microscope. Primary electron beam displacement, caused by surface charges, can be then measured for every grid knot. Using geometric parameters of the setup, a quantitative mapping of the potential can be extracted. It is shown that this method can achieve a tens of millivolt sensitivity and a submicron spatial resolution in electrostatic potential measurements.
Differential Expression of Virulence and Stress Fitness Genes between
Escherichia coli
O157:H7 Strains with Clinical or Bovine-Biased Genotypes
Authors: Vanaja Sivapriya Kailasan , Springman Amber C. , Besser Thomas E. , Whittam Thomas S. , Manning Shannon D.
Published: October 2009

Escherichia coli
O157:H7 strains can be classified into different genotypes based on the presence of specific Shiga toxin-encoding bacteriophage insertion sites. Certain O157:H7 genotypes predominate among human clinical cases (clinical genotypes), while others are more frequently found in bovines (bovine-biased genotypes). To determine whether inherent differences in gene expression explain the variation in infectivity of these genotypes, we compared the expression patterns of clinical genotype 1 strains with those of bovine-biased genotype 5 strains using microarrays. Important O157:H7 virulence factors, including locus of enterocyte effacement genes, the enterohemolysin, and several pO157 genes, showed increased expression in the clinical versus bovine-biased genotypes. In contrast, genes essential for acid resistance (e.g.,
gadA
,
gadB
, and
gadC
) and stress fitness were upregulated in bovine-biased genotype 5 strains. Increased expression of acid resistance genes was confirmed functionally using a model stomach assay, in which strains of bovine-biased genotype 5 had a 2-fold-higher survival rate than strains of clinical genotype 1. Overall, these results suggest that the increased prevalence of O157:H7 illness caused by clinical genotype 1 strains is due in part to the overexpression of key virulence genes. The bovine-biased genotype 5 strains, however, are more resistant to adverse environmental conditions, a characteristic that likely facilitates O157:H7 colonization of bovines.
Roles of the Snf1-Activating Kinases during Nitrogen Limitation and Pseudohyphal Differentiation in
Saccharomyces cerevisiae
Authors: Orlova Marianna , Ozcetin Hamit , Barrett LaKisha , Kuchin Sergei
Published: October 2009

In
Saccharomyces cerevisiae
, Snf1 protein kinase is important for growth on carbon sources that are less preferred than glucose. When glucose becomes limiting, Snf1 undergoes catalytic activation, which requires phosphorylation of its T-loop threonine (Thr210). Thr210 phosphorylation can be performed by any of three Snf1-activating kinases: Sak1, Tos3, and Elm1. These kinases are redundant in that all three must be eliminated to confer
snf1
Δ-like growth defects on nonpreferred carbon sources. We previously showed that in addition to glucose signaling, Snf1 also participates in nitrogen signaling and is required for diploid pseudohyphal differentiation, a filamentous-growth response to nitrogen limitation. Here, we addressed the roles of the Snf1-activating kinases in this process. Loss of Sak1 caused a defect in pseudohyphal differentiation, whereas Tos3 and Elm1 were dispensable. Sak1 was also required for increased Thr210 phosphorylation of Snf1 under nitrogen-limiting conditions. Expression of a catalytically hyperactive version of Snf1 restored pseudohyphal differentiation in the
sak1
Δ/
sak1
Δ mutant. Thus, while the Snf1-activating kinases exhibit redundancy for growth on nonpreferred carbon sources, the loss of Sak1 alone produced a significant defect in a nitrogen-regulated phenotype, and this defect resulted from deficient Snf1 activation rather than from disruption of another pathway. Our results suggest that Sak1 is involved in nitrogen signaling upstream of Snf1.
The Silicon Layer Supports Acid Resistance of
Bacillus cereus
Spores
Authors: Hirota Ryuichi , Hata Yumehiro , Ikeda Takeshi , Ishida Takenori , Kuroda Akio
Published: October 2009

Silicon (Si) is considered to be a “quasiessential” element for most living organisms. However, silicate uptake in bacteria and its physiological functions have remained obscure. We observed that Si is deposited in a spore coat layer of nanometer-sized particles in
Bacillus cereus
and that the Si layer enhances acid resistance. The novel acid resistance of the spore mediated by Si encapsulation was also observed in other
Bacillus
strains, representing a general adaptation enhancing survival under acidic conditions.
Thermococcus kodakar
ensis
Mutants Deficient in Di-
myo
-Inositol Phosphate Use Aspartate To Cope with Heat Stress
Authors: Borges Nuno , Matsumi Rie , Imanaka Tadayuki , Atomi Haruyuki , Santos Helena
Published: October 2009

Many of the marine microorganisms which are adapted to grow at temperatures above 80°C accumulate di-
myo
-inositol phosphate (DIP) in response to heat stress. This led to the hypothesis that the solute plays a role in thermoprotection, but there is a lack of definitive experimental evidence. Mutant strains of
Thermococcus kodakar
ensis
(formerly
Thermococcus kodakaraensis
), manipulated in their ability to synthesize DIP, were constructed and used to investigate the involvement of DIP in thermoadaptation of this archaeon. The solute pool of the parental strain comprised DIP, aspartate, and α-glutamate. Under heat stress the level of DIP increased 20-fold compared to optimal conditions, whereas the pool of aspartate increased 4.3-fold in response to osmotic stress. Deleting the gene encoding the key enzyme in DIP synthesis, CTP:inositol-1-phosphate cytidylyltransferase/CDP-inositol:inositol-1-phosphate transferase, abolished DIP synthesis. Conversely, overexpression of the same gene resulted in a mutant with restored ability to synthesize DIP. Despite the absence of DIP in the deletion mutant, this strain exhibited growth parameters similar to those of the parental strain, both at optimal (85°C) and supraoptimal (93.7°C) temperatures for growth. Analysis of the respective solute pools showed that DIP was replaced by aspartate. We conclude that DIP is part of the strategy used by
T. kodakarensis
to cope with heat stress, and aspartate can be used as an alternative solute of similar efficacy. This is the first study using mutants to demonstrate the involvement of compatible solutes in the thermoadaptation of (hyper)thermophilic organisms.
Endogenous Phenazine Antibiotics Promote Anaerobic Survival of
Pseudomonas aeruginosa
via Extracellular Electron Transfer
Authors: Wang Yun , Kern Suzanne E. , Newman Dianne K.
Published: October 2009

Antibiotics are increasingly recognized as having other, important physiological functions for the cells that produce them. An example of this is the effect that phenazines have on signaling and community development for
Pseudomonas aeruginosa
(L. E. Dietrich, T. K. Teal, A. Price-Whelan, and D. K. Newman, Science 321:1203-1206, 2008). Here we show that phenazine-facilitated electron transfer to poised-potential electrodes promotes anaerobic survival but not growth of
Pseudomonas aeruginosa
PA14 under conditions of oxidant limitation. Other electron shuttles that are reduced but not made by PA14 do not facilitate survival, suggesting that the survival effect is specific to endogenous phenazines.
Implication of Serine Residues 271, 273, and 275 in the Human Immunodeficiency Virus Type 1 Cofactor Activity of Lens Epithelium-Derived Growth Factor/p75
Authors: Garcia-Rivera Jose A. , Bueno Murilo T. D. , Morales Elisa , Kugelman Jeffrey R. , Rodriguez Daniel F. , Llano Manuel
Published: November 2009

Lens epithelium-derived growth factor (LEDGF)/p75 is a cellular cofactor for HIV-1 DNA integration. It is well established that the simultaneous binding of LEDGF/p75 to chromatin and to HIV-1 integrase is required for its cofactor activity. However, the exact molecular mechanism of LEDGF/p75 in HIV-1 integration is not yet completely understood. Our hypothesis is that evolutionarily conserved regions in LEDGF/p75 exposed to solvent and harboring posttranslational modifications may be involved in its HIV-1 cofactor activity. Therefore, a panel of LEDGF/p75 deletion mutants targeting these protein regions were evaluated for their HIV-1 cofactor activity, chromatin binding, integrase interaction, and integrase-to-chromatin-tethering activity by using different cellular and biochemical approaches. The deletion of amino acids 267 to 281 reduced the cofactor activity of LEDGF/p75 to levels observed for chromatin-binding-defective mutants. This region contains a serine cluster (residues 271, 273, and 275) recurrently found to be phosphorylated in both human and mouse cells. Importantly, the conversion of these Ser residues to Ala was sufficient to impair the ability of LEDGF/p75 to mediate HIV-1 DNA integration, although these mutations did not alter chromatin binding, integrase binding, or the integrase-to-chromatin-tethering capability of LEDGF/p75. These results clearly indicated that serine residues 271, 273, and 275 influence the HIV-1 cofactor activity of integrase-to-chromatin-tethering-competent LEDGF/p75.
Integrity of the Early Secretory Pathway Promotes, but Is Not Required for, Severe Acute Respiratory Syndrome Coronavirus RNA Synthesis and Virus-Induced Remodeling of Endoplasmic Reticulum Membranes
Authors: Knoops Kèvin , Swett-Tapia Cindy , van den Worm Sjoerd H. E. , te Velthuis Aartjan J. W. , Koster Abraham J. , Mommaas A. Mieke , Snijder Eric J. , Kikkert Marjolein
Published: November 2009

To accommodate its RNA synthesis in the infected cell, severe acute respiratory syndrome coronavirus (SARS-CoV) induces a cytoplasmic reticulovesicular network (RVN) that is derived from endoplasmic reticulum (ER) membranes. We set out to investigate how the early secretory pathway interacts with the RVN and the viral replication/transcription complex (RTC) that is anchored to it. When the secretory pathway was disrupted by brefeldin A (BFA) treatment at the start of infection, RVN formation and viral RTC activity were not blocked and continued up to 11 h postinfection, although RNA synthesis was reduced by ca. 80%. In vitro RTC assays, using membrane fractions from infected cells, demonstrated that BFA does not directly interfere with the activity of the viral RNA-synthesizing enzymes. Confocal microscopy studies showed that early secretory pathway components are not associated with SARS-CoV-induced replication sites, although our studies revealed that infection induces a remarkable redistribution of the translocon subunit Sec61α. Ultrastructural studies, including electron tomography, revealed that the formation of the RVN and all its previously documented features can occur in the presence of BFA, despite differences in the volume and morphology of the network. We therefore conclude that early secretory pathway proteins do not play a direct role in RVN morphogenesis or the functionality of the SARS-CoV RTC. The BFA-induced disruption of ER integrity and functionality probably affects the overall quality of the membrane scaffold that is needed to support the viral RTC and/or the availability of specific host factors, which in turn compromises viral RNA synthesis.
In-Depth Analysis of Kaposi's Sarcoma-Associated Herpesvirus MicroRNA Expression Provides Insights into the Mammalian MicroRNA-Processing Machinery
Authors: Umbach Jennifer L. , Cullen Bryan R.
Published: November 2009

We have used deep sequencing to analyze the pattern of viral microRNA (miRNA) expression observed in the B-cell line BC-3, which is latently infected with Kaposi's sarcoma-associated herpesvirus (KSHV). We recovered 14.6 × 10
6
total miRNA cDNA reads, of which a remarkable 92% were of KSHV origin. We detected 11 KSHV miRNAs as well as all 11 predicted miRNA* or passenger strands from the miRNA duplex intermediate. One previously reported KSHV miRNA, miR-K9, was found to be mutationally inactivated. This analysis revealed that the 5′ ends of 10 of the 11 KSHV miRNAs were essentially invariant, with significantly more variation being observed at the 3′ end, a result which is consistent with the proposal that the 5′-proximal region of miRNAs is critical for target mRNA recognition. However, one KSHV miRNA, miR-K10-3p, was detected in two isoforms differing by 1 nucleotide (nt) at the 5′ end that were present at comparable levels, and these two related KSHV miRNAs are therefore likely to target at least partially distinct mRNA populations. Finally, we also report the first detection of miRNA offset RNAs (moRs) in vertebrate somatic cells. moRs, which derive from primary miRNA (pri-miRNA) sequences that immediately flank the mature miRNA and miRNA* strands, were identified flanking one or both sides of nine of the KSHV miRNAs. These data provide new insights into the pattern of miRNA processing in mammalian cells and indicate that this process is highly conserved during animal evolution.
Safety of intravenous heparin administration after endovascular treatment for ruptured intracranial aneurysms
Authors: Vance A Z , Jayaraman M V , Dubel G J , Doberstein C E , Haas R A
Published: October 2009

Introduction

Thromboembolic events are the primary complications encountered during endovascular treatment (EVT) of intracranial aneurysms. Intraprocedural heparinization is common during EVT but is less common post-procedure. The safety of heparinization following EVT is unknown, especially for ruptured aneurysms.

Materials and methods

The records of 138 consecutive patients at our institution from 1 January 2000 to 30 June 2007 who were treated with EVT for 140 ruptured intracranial aneurysms were reviewed. All patients were treated with low dose intravenous heparin post-procedure for 24 h as per the departmental protocol. Cases of worsening hemorrhage requiring surgical evacuation were considered significant hemorrhages. Prior surgical exploration and external ventricular drain (EVD) placement were also noted.

Results

There were two cases (1.4%) of significant worsening hemorrhage during post-procedure heparin administration. Among 13 patients who underwent craniotomy (for hematoma evacuation or attempted surgical clipping) prior to EVT, there was one (7.7%) case of significant hemorrhage. Among the 60 patients who underwent EVD placement prior to EVT, there was one (1.7%) case of significant hemorrhage.

Conclusion

Administration of systemic heparinization may be safe during the first 24 h post-EVT of a ruptured intracranial aneurysm in patients without recent craniotomy. Further study in determining the benefit of this protocol in reducing post-embolization thromboembolic complications may be warranted.
Invasive zygomycosis in India: experience in a tertiary care hospital
Authors: Chakrabarti A , Chatterjee S S , Das A , Panda N , Shivaprakash M R , Kaur A , Varma S C , Singhi S , Bhansali A , Sakhuja V
Published: November 2009

Aim

To report the natural history and clinical course of zygomycosis from a single tertiary care centre in India where doctors maintain an institutional zygomycosis registry.

Methods

The clinical and laboratory data collected prospectively from patients with antemortem diagnosis for invasive zygomycosis, and retrospectively from autopsy diagnosed cases, over an 18 month period (July 2006–December 2007) were combined and analysed.

Results

During the period 75 cases (50 cases/year) of zygomycosis were reported. Antemortem diagnosis could be made in 81% of cases and 9% of patients had nosocomial zygomycosis. The spectrum of disease included rhino-orbito-cerebral (48%), pulmonary (17%), gastrointestinal (13%), cutaneous (11%), renal and disseminated zygomycosis (5% each). Uncontrolled type 2 diabetes (58%) and diabetic ketoacidosis (38%) in the rhino-orbito-cerebral type, renal failure (69%) in the pulmonary type, prematurity (70%) in the gastrointestinal type, and breach of skin (88%) in cutaneous zygomycosis, were the significant (p<0.05) underlying illnesses. Rhizopus oryzae (69%) was the most common isolate followed by Apophysomyces elegans (19%). Overall mortality was 45% in patients who could be treated. Outcome was significantly poor when surgical debridement could not be performed or the patients were treated only with amphotericin B deoxycholate. On multivariate analysis, patients with a Glasgow Coma Score (GCS) ⩾9 had a better prognosis.

Conclusions

Zygomycosis is a threat in uncontrolled diabetes. New risk factors such as renal failure and chronic liver disease require attention. A elegans is an emerging agent in India. The need for surgical debridement in addition to medical treatment is emphasised. GCS is an independent marker of prognosis in cases of invasive zygomycosis.
The life history of Palmaria palmata in culture. A new type for the Rhodophyta
Authors: van derMeer John P. , Todd Edna R.
Published: November 2009

The life history of Palmaria palmata has been completed in culture. Tetraspores from diploid plants gave rise to male and female haploid plants which differed morphologically. Female plants were extremely small and became sexually mature only days after tetraspore release. Trichogynes were observed on plants only 4 days old, and remained conspicuous for several weeks. As the females aged, trichogynes declined in number and they could not be detected on plants 5 months old. In contrast, male plants required several (9–12) months of vegetative growth before they formed spermatia. As a consequence, females had to be fertilized by older males from preceding gametangial generations.The diploid tetrasporangial plants developed directly on fertilized females. As they enlarged, they completely overgrew the small females and formed their own holdfast attachments to the substrate. A recessive mutation resulting in green frond colour was used in crosses designed to yield red diploid tissue on green females after fertilization, thereby greatly facilitating observations on the development of the tetrasporangial phase.Preliminary observations indicate that the carpogonium is a single cell. There appears to be no carpogonial branch or auxilliary cell. The tetrasporangial phase develops from the zygote by simple mitotic divisions, suggesting that the life history is best interpreted as lacking a carposporophyte.
Studies on the growth of Frankia isolates in relation to infectivity and nitrogen fixation (acetylene reduction)
Authors: Burggraaf A. J. P. , Shipton W. A.
Published: November 2009

Several Frankia isolates were tested for their growth ability on a mineral medium containing glucose, succinic acid, or propionic acid as the sole carbon–energy source. Utilization of these nutrients allowed a preliminary discrimination between isolates. Propionic acid turned out to be a rather universal carbon source for the isolates involved in this study. In a system containing propionic acid as C–energy source and NH4Cl as N source, the development of infectivity on A. glutinosa with free-living cultures of CpI1 was followed during a growth period of 30 days. The growth pattern was compared with the development of both infective and viable units and the number of hyphal units and spores counted in mildly sonicated samples. On the same medium without NH4Cl several isolates were studied for the development of nitrogenase activity (acetylene reduction) in a growth experiment. The relation between growth and nitrogen fixation was also studied and compared in some experiments with the development of vesicles.
Seasonal pattern of energy use, respiration, and nitrogenase activity in root nodules of Myrica gale
Authors: Schwintzer Christa R. , Tjepkema John D.
Published: November 2009

Annual CO2 evolution, H2 evolution, and C2H2 reduction were measured in root nodules from a vigorous Myrica gale stand in a Massachusetts peatland at 3-week intervals in 1980. Nodule activity was approximately the same under the experimental conditions (excised nodules reducing C2H2) as in nature (attached nodules reducing N2) and the CO2 evolution to O2 uptake ratio averaged 1.07. Nitrogenase activity was first detectable in late May, reached its maximum [Formula: see text] in mid-July, and disappeared in late October. The seasonal pattern of CO2 evolution was similar except that it continued at low rates when nitrogenase activity was absent. Hydrogen evolution was barely detectable. The energy cost of nitrogen fixation, expressed as the molar CO2:C2H4 ratio, was relatively low [Formula: see text] throughout the period of substantial nitrogenase activity and had a mean annual value of 4.9. Annual N2 fixation was estimated to be 2.8 g N m−2year−1, contributing about 33% of the annual N requirement measured in 1979. Annual C use by nodules was about 21.0 g C m−2 year−1. If this C were available for additional net production, it would increase it by about 5.5%.
Postglacial vegetational change and soil development in southeastern Labrador as inferred from pollen and chemical stratigraphy
Authors: Engstrom D. R. , Hansen B. C. S.
Published: November 2009

Palynological and geochemical analyses of Holocene lake sediments are used to evaluate long-term interactions between vegetation and soils from four sites in southeastern Labrador, Canada. Changes in soil composition are inferred from the stratigraphy of humic materials and the elemental composition of authigenic and allogenic fractions of the sediment. Early Holocene lake muds deposited under tundra vegetation are predominantly inorganic and contain high concentrations of allogenic elastics derived from the erosion of barren soils. Concentrations of humic materials and redox–pH-sensitive elements (Fe, Mn, P, Al) of authigenic origin increase markedly with the subsequent invasion of spruce and fir (8000–7000 years BP). These changes represent decreased erosion of clastic minerals and increased mobilization of organometallic complexes from waterlogged soils produced through humus accumulation under coniferous vegetation. This transition of inorganic tundra inceptisols to humic-rich boreal spodosols contributed to the competitive replacement of Picea glauca and Abies balsamea by the more edaphically tolerant P. mariana between 6500 and 6000 years BP. A subsequent decline in sedimentary humic content and increase in allogenic components may signal a regional climatic cooling after 4000 years BP. Geochemical analyses of lake sediments reveal no stratigraphic changes in allogenic mineral composition that might indicate progressive soil weathering.
DEPENDENCE OF THE DAVYDOV'S SOLITON BEHAVIOR IN THE LINEAR POLYMER CHAIN ON THE EXCITON–PHONON COUPLING
Authors: TODOROVIĆ DRAGAN , PANTIĆ MILAN , ŠKRINJAR MARIO , KAPOR DARKO , STOJANOVIĆ STANOJE
Published: November 2009

The Davydov's soliton propagation in the linear polymer chain is analyzed numerically by solving the discrete equations of motion for exciton and phonon amplitudes. The main difference with respect to the results of continual approximation is that two exciton–phonon coupling constants influence separately the soliton behavior. Their influence is studied both in the ideal chain and the chain with single impurity.
Acheron, a Lupus antigen family member, regulates integrin expression, adhesion, and motility in differentiating myoblasts
Authors: Glenn Honor L. , Wang Zhaohui , Schwartz Lawrence M.
Published: November 2009

Acheron (Achn) was originally identified as novel gene that is induced when insect muscles become committed to die at the end of metamorphosis. In separate studies, we have demonstrated that Achn acts upstream of MyoD and is required by mammalian myoblasts to either differentiate or undergo apoptosis following loss of growth factors. In the present study we examined the role of Achn in regulating integrin-extracellular matrix interactions that are required for myogenesis. Both control C2C12 myoblasts and those engineered to express ectopic Achn expressed the fibronectin receptor integrin α5β1 in the presence of growth factors and the laminin receptor α7β1 following growth factor withdrawal. Expression of the laminin receptor was blocked in cells expressing either Achn antisense or an Achn deletion mutant that blocks differentiation. Control cells and those expressing ectopic Achn undergo sequential and transient increases in both substrate adhesion and migration before cell fusion. Blockade of Achn expression reduced these effects on laminin but not on fibronectin. Taken together, these data suggest that Achn may influence differentiation in part via its control of cell adhesion dynamics.
Angiotensin II exerts glucose-dependent effects on Kvcurrents in mouse pancreatic β-cells via angiotensin II type 2 receptors
Authors: Chu Kwan Yi , Cheng Qianni , Chen Chen , Au Lai Shan , Seto Sai Wang , Tuo Ya , Motin Leonid , Kwan Yiu Wa , Leung Po Sing
Published: November 2009

Hyperglycemia-associated glucotoxicity induces β-cell apoptosis but the underlying mechanisms are unknown. Interestingly, prolonged exposure to high glucose upregulates the expression and function of the renin-angiotensin system (RAS). We hypothesize that the voltage-gated outward potassium (Kv) current, which governs β-cell membrane potential and insulin secretion, has a role in glucotoxicity. In this study, we investigated the effects of prolonged exposure to high glucose on mouse pancreatic β-cells and concurrent effects on the RAS by examining changes in expression of angiotensin II (ANG II) receptors and changes in the expression and activity of Kvchannels. β-Cells were incubated in high glucose medium for 1–7 days and then were examined with electrophysiological and molecular biology techniques. Prolonged exposure to high glucose produced a marked increase in β-cell primary Kvchannel subunit, Kv2.1, expression and Kvcurrent amplitude. Enhanced expression of ANG II type 1 receptor (AT1R) was also observed under high glucose conditions, whereas blockade of AT1R by losartan did not alter Kvchannel expression. External application of ANG II reduced Kvcurrent amplitude under normal, but not high, glucose conditions. The effect of ANG II on Kvchannel gating was abolished by ANG II type 2 receptor (AT2R) antagonism. These data suggest that hyperglycemia alters β-cell function through modification of the Kvchannel which may be associated with the RAS.
Complex interactions of NO/cGMP/PKG systems on Ca2+signaling in afferent arteriolar vascular smooth muscle
Authors: Fellner Susan K. , Arendshorst William J.
Published: October 2009

Little is known about the effects of nitric oxide (NO) and the cyclic GMP (cGMP)/protein kinase G (PKG) system on Ca2+signaling in vascular smooth muscle cells (VSMC) of resistance vessels in general and afferent arterioles in particular. We tested the hypotheses that cGMP-, Ca2+-dependent big potassium channels (BKCa2+) buffer the Ca2+response to depolarization by high extracellular KCl and that NO inhibits adenosine diphosphoribose (ADPR) cyclase, thereby reducing the Ca2+-induced Ca2+release. We isolated rat afferent arterioles, utilizing the magnetized microsphere method, and measured cytosolic Ca2+concentration ([Ca2+]i) with fura-2, a preparation in which endothelial cells do not participate in [Ca2+]iresponses. KCl (50 mM)-induced depolarization causes an immediate increase in [Ca2+]iof 151 nM. The blockers Nω-nitro-l-arginine methyl ester (of nitric oxide synthase), 1,2,4-oxodiazolo-[4,3- a]quinoxalin-1-one (ODQ, of guanylyl cyclase), KT-5823 (of PKG activation), and iberiotoxin (IBX, of BKCa2+activity) do not alter the [Ca2+]iresponse to KCl, suggesting no discernible endogenous NO production under basal conditions. The NO donor sodium nitroprusside (SNP) reduces the [Ca2+]iresponse to 77 nM; IBX restores the response to control values. These data show that activation of BKCa2+in the presence of NO/cGMP provides a brake on KCl-induced [Ca2+]iresponses. Experiments with the inhibitor of cyclic ADPR 8-bromo-cyclic ADPR (8-Br-cADPR) and SNP + downstream inhibitors of PKG and BKCa2+suggest that NO inhibits ADPR cyclase in intact arterioles. When we pretreat afferent arterioles with 8-bromoguanosine 3′,5′-cyclic monophosphate (8-Br-cGMP; 10 μM), the response to KCl is 143 nM. However, in the presence of both IBX and 8-Br-cGMP, we observe a surprising doubling of the [Ca2+]iresponse to KCl. In summary, we present evidence for effects of the NO/cGMP/PKG system to reduce [Ca2+]i, via activation of BKCa2+and possibly by inhibition of ADPR cyclase, and to increase [Ca2+]i, by a mechanism(s) yet to be defined.
Ischemic preconditioning and heat shock activate Akt via a focal adhesion kinase-mediated pathway in Langendorff-perfused adult rat hearts
Authors: Wei Hongguang , Vander Heide Richard S.
Published: October 2009

Heat stress (HS)-induced cardioprotection is associated with the activation of focal adhesion kinase (FAK) and protein kinase B (Akt) in neonatal rat ventricular myocytes (NRVMs), suggesting that stress-induced activation of survival pathways may be important in protecting intact hearts from irreversible injury. The purposes of this study were 1) to examine the subcellular signaling pathways activated by HS and ischemic preconditioning (IP) in intact hearts, 2) to determine whether HS and IP activate an integrated survival pathway similar to that activated by HS in cultured NRVMs, and 3) to determine whether HS and IP reduce lethal cell injury in perfused intact hearts. Adult rat hearts perfused in the Langendorff mode were subjected to 25 min of global ischemia and 30 min of reperfusion (I/R) either 24 h after whole animal HS or following a standard IP protocol. Myocardial signaling was analyzed using Western blot analysis, whereas cell death was assayed by measuring lactate dehydrogenase release into the perfusate and confirmed by light microscopy. Similar to NRVMs, HS performed in the whole animal 24 h before I/R increased phosphorylation of FAK at tyrosine-397 and protein kinase B (Akt) and resulted in protection from cell death. Using IP as a myocardial stress also resulted in an increased phosphorylation/activation of both FAK and Akt and resulted in reduced cell death in adult perfused rat hearts subjected to I/R. In conclusion, 1) myocardial stress caused by whole animal HS activates cytoskeletal-based survival signaling pathways in whole heart tissue and reduces lethal I/R injury and 2) IP activates the same stress-induced survival pathway and the activation correlates with the well-known cardioprotective effect of IP on lethal I/R injury.
Interstitial flow induces MMP-1 expression and vascular SMC migration in collagen I gels via an ERK1/2-dependent and c-Jun-mediated mechanism
Authors: Shi Zhong-Dong , Ji Xin-Ying , Berardi Danielle E. , Qazi Henry , Tarbell John M.
Published: October 2009

The migration of vascular smooth muscle cells (SMCs) and fibroblasts into the intima after vascular injury is a central process in vascular lesion formation. The elevation of transmural interstitial flow is also observed after damage to the vascular endothelium. We have previously shown that interstitial flow upregulates matrix metalloproteinase-1 (MMP-1) expression, which in turn promotes SMC and fibroblast migration in collagen I gels. In this study, we investigated further the mechanism of flow-induced MMP-1 expression. An ERK1/2 inhibitor PD-98059 completely abolished interstitial flow-induced SMC migration and MMP-1 expression. Interstitial flow promoted ERK1/2 phosphorylation, whereas PD-98059 abolished flow-induced activation. Silencing ERK1/2 completely abolished MMP-1 expression and SMC migration. In addition, interstitial flow increased the expression of activator protein-1 transcription factors (c-Jun and c-Fos), whereas PD-98059 attenuated flow-induced expression. Knocking down c- jun completely abolished flow-induced MMP-1 expression, whereas silencing c- fos did not affect MMP-1 expression. Taken together, our data indicate that interstitial flow induces MMP-1 expression and SMC migration in collagen I gels via an ERK1/2-dependent and c-Jun-mediated mechanism and suggest that interstitial flow, ERK1/2 MAPK, c-Jun, and MMP-1 may play important roles in SMC migration and neointima formation after vascular injury.
Bone marrow-derived progenitor cells prevent thrombin-induced increase in lung vascular permeability
Authors: Zhao Yidan D. , Ohkawara Hiroshi , Vogel Stephen M. , Malik Asrar B. , Zhao You-Yang
Published: October 2009

Since thrombin activation of endothelial cells (ECs) is well-known to increase endothelial permeability by disassembly of adherens junctions (AJs) and actinomyosin contractility mechanism involving myosin light chain (MLC) phosphorylation, we investigated the effects of bone marrow-derived progenitor cells (BMPCs) on the thrombin-induced endothelial permeability response. We observed that addition of BMPCs to endothelial monolayers at a fixed ratio prevented the thrombin-induced decrease in transendothelial electrical resistance, a measure of AJ integrity, and increased mouse pulmonary microvessel filtration coefficient, a measure of transvascular liquid permeability. The barrier protection was coupled to increased vascular endothelial cadherin expression and increased Cdc42 activity in ECs. Using small interfering RNA (siRNA) to deplete Cdc42 in ECs, we demonstrated a key role of Cdc42 in signaling the BMPC-induced endothelial barrier protection. Endothelial integrity induced by BMPCs was also secondary to inhibition of MLC phosphorylation in ECs. Thus BMPCs interacting with ECs prevent thrombin-induced endothelial hyperpermeability by a mechanism involving AJ barrier annealing, inhibition of MLC phosphorylation, and activation of Cdc42.
Sympathetic activity is not increased inl-NAME hypertensive rats
Authors: dos Santos Fernanda Machado , Martins Dias Daniel Penteado , da Silva Carlos Alberto Aguiar , Fazan Rubens , Salgado Helio Cesar
Published: November 2009

The role played by the sympathetic drive in the development of NG-nitro-l-arginine methyl ester (l-NAME)-induced hypertension is not firmly established. Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with l-NAME over the course of either 2 or 14 days. Mean arterial pressure (MAP) was measured via a catheter placed in the femoral artery, drugs were administered via a cannula placed in the femoral vein, and renal sympathetic nerve activity (RSNA) was monitored using an implanted electrode. Despite the remarkable increase in arterial pressure, heart rate did not change after treatment with l-NAME. RSNA was similar in l-NAME-induced hypertensive rats treated over the course of 2 or 14 days, as well as in normotensive rats. It was also demonstrated that l-NAME-induced hypertensive rats displayed a resetting of the baroreflex control of RSNA to hypertensive levels, with decreased sensitivity over the course of 2 or 14 days. Furthermore, the sympathetic-vagal balance examined in the time and frequency domain and the renal and plasma norepinephrine content did not differ between groups. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by l-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity.
The Development of a Simple Risk Score to Predict Early Outcome in Severe Acute Acidotic Cardiogenic Pulmonary Edema
Authors: Gray Alasdair , Goodacre Steve , Nicholl Jon , Masson Moyra , Sampson Fiona , Elliott Mark , Crane Steve , Newby Dave E.
Published: October 2009

Background—

Acute cardiogenic pulmonary edema is a common medical emergency with high early mortality. Initial clinical assessment would benefit from accurate mortality prediction. We aimed to develop a simple clinical score based on presenting characteristics that would predict 7-day mortality in patients with acute cardiogenic pulmonary edema.

Methods and Results—

We used data from patients recruited to the 3CPO trial (a pragmatic multicenter trial comparing continuous positive airway pressure, noninvasive positive pressure ventilation, and standard oxygen therapy in emergency department patients with acute cardiogenic pulmonary edema) to investigate the association between baseline characteristics and 7-day mortality. Factors associated with mortality (
P
<0.1) were entered into a multivariable model. Independent predictors of mortality from the multivariable model (
P
<0.05) were assigned integer weights based on their coefficients and incorporated into a risk score. The discriminant ability of the score was tested by receiver operator characteristic analysis. Data from 1069 patients (78±10 years; 43% men; 7-day mortality, 9.6%) were analyzed. Multivariable analysis identified age (
P
=0.003), systolic blood pressure (
P
<0.001), and Glasgow Coma Scale motor component dichotomized and simplified to the ability to obey commands or not (
P
=0.02) as the only independent predictors of 7-day mortality. These were weighted and used to develop a risk score ranging from 0 (7-day mortality, 1.9%; 95% CI, 0.8 to 4.5) to 7 (7-day mortality, 100%; 95% CI, 34.2 to 100). Receiver operator characteristic analysis demonstrated good risk prediction with a c-statistic of 0.794 (95% CI, 0.745 to 0.843). A simplified 3-point score with no weighting had a c-statistic of 0.754 (95% CI, 0.701 to 0.807).

Conclusions—

A simple clinical score based on age, systolic blood pressure, and the ability to obey commands predicts early mortality in patients with acute cardiogenic pulmonary edema.

Clinical Trial Registration—

clinicaltrials.gov Identifier: ISRCTN077448447.
At Whose Table? Stories of Elites and Social Climbers in 1-2 Samuel
Authors: Hamilton Mark
Published: November 2009

1-2 Samuel and indeed the entire Deuteronomistic History include several stories of elite members of society and their lifeways, concentrating on their use of economic resources, proper self-display as rhetors, and obedience or otherwise to those around them. Like other traditional societies, ancient Israel had a fairly deeply articulated sense of appropriate behavior by such persons. This paper draws on contemporary studies in both anthropology and rhetoric, as well as comparative evidence from the ancient Near East and other Israelite texts, to examine the stories of Nabal (1 Sam 25) and Barzillai (2 Sam 19) in their ancient social settings and locations in 2 Samuel. It argues that stories of such landed gentry reflect the interests of the readers and authors of these texts and reveal part of the social location of the entire DH. As such, they allow us to question a simplistic attribution of these texts either to the royal court or its critics, illustrating the complex interrelationships among various settings in Israelite life.
Balliol 63 and Parisian Theology around 1320
Authors: Courtenay William
Published: November 2009

The article provides a survey of the content of Balliol College 63, with special attention to the questions of Gerard of Siena. It establishes that many of the texts in the first half of the manuscript (ff. 1r-88v) are pre-edited versions written at Paris in the 1317-1321 period. To illustrate that point, Gerard of Siena's question on whether the articles of faith are the principles of theology is edited in the appendices in its pre-edited (Balliol 63) and final form as edited by Gerard in the 1320s.