bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Dynamics of Idealized Convection Schemes and Their Effect on the Zonally Averaged Tropical Circulation
Authors: Frierson Dargan M. W. 
Published: June 2007

In this paper, the effect of a simple convection scheme on the zonally averaged tropical general circulation is examined within an idealized moist GCM to obtain broad classifications of the influence of convection on the Tropics. This is accomplished with a simplified convection scheme in the style of Betts and Miller. The scheme is utilized in a moist GCM with simplified physical parameterizations (gray radiation, with zonally symmetric, slab mixed layer ocean boundary conditions). Comparisons are made with simulations without a convection scheme [i.e., with large-scale condensation (LSC) only], with the moist convective adjustment (MCA) parameterization, and with various formulations and parameter sets with a simplified Betts–Miller (SBM) scheme. With the control run using the SBM scheme, the Tropics become quieter and less dependent on horizontal resolution as compared with the LSC or MCA simulations. The Hadley circulation mass transport is significantly reduced with the SBM scheme, as is the ITCZ precipitation. An important factor determining this behavior is the parameterization of shallow convection: without shallow convection, the convection scheme is largely ineffective at preventing convection from occurring at the grid scale. The sensitivities to convection scheme parameters are also examined. The simulations are remarkably insensitive to the convective relaxation time, and only mildly sensitive to the relative humidity of the reference profile, provided significant large-scale condensation is not allowed to occur. The changes in the zonally averaged tropical circulation that occur in all the simulations are understood based on the convective criteria of the schemes and the gross moist stability of the atmosphere.
Convectively Coupled Kelvin Waves in an Idealized Moist General Circulation Model
Authors: Frierson Dargan M. W. 
Published: June 2007

The dynamics of convectively coupled Kelvin waves and their dependence on convection scheme parameters are studied within a simplified moist general circulation model. The model consists of the primitive equations on the sphere over zonally symmetric aquaplanet, slab mixed layer ocean boundary conditions, and idealized physical parameterizations including gray radiative transfer and a simplified Betts–Miller convection scheme. This framework allows the authors to study the dependence of Kelvin waves on quantities such as the gross moist stability in a clean manner. A control simulation with the model produces convectively coupled Kelvin waves that are remarkably persistent and dominate the variability within the Tropics. These waves propagate with an equivalent depth of ≈40 m. Linear regression analysis with respect to a Kelvin-filtered time series shows that the waves are driven by evaporation–wind feedback and have structures broadly consistent with theoretical predictions for Kelvin waves. Next, the determination of the speed and structure of the Kelvin waves is studied by examining the response of the waves to changes in convection scheme parameters. When the convective relaxation time is lengthened, the waves are damped and eventually are completely eliminated. The propagation speed additionally increases with longer relaxation time. Then changes to a convection scheme parameter that essentially controls the fraction of convective versus large-scale precipitation are examined. When some large-scale precipitation occurs, the waves increase in strength, propagate more slowly, and move to larger scales. However, when mostly large-scale precipitation occurs, the Kelvin wave disappears, and the Tropics are dominated by tropical storm–like variability. The decrease in speed is related here to the gross moist stability of the atmosphere, which is reduced with increased large-scale precipitation.
Decreased Pulsatile Blood Flow in the Patella in Patellofemoral Pain Syndrome
Authors: Näslund Jan , Walden Markus , Lindberg Lars-Göran 
Published: June 2007

Background Anterior knee pain without clinical and radiologic abnormalities has primarily been explained from a purely structural view. A recently proposed biologic and homeostatic explanation questions the malalignment theory. No objective measurement of the pathophysiology responsible for changes in local homeostasis has been presented. Hypothesis Flexing the knee joint interferes with the perfusion of the patellar bone in patellofemoral pain syndrome. Study Design Case control study; Level of evidence, 4. Methods Pulsatile blood flow in the patella was measured continuously and noninvasively using photoplethysmography. Measurements were made with the patient in a resting position with knee flexion of 20° and after passive knee flexion to 90°. In total, 22 patients with patellofemoral pain syndrome were examined bilaterally, and 33 subjects with healthy knees served as controls. Results The pulsatile blood flow in the patient group decreased after passive knee flexion from 20° to 90° (systematic change in position, or relative position [RP] = —0.32; 95% confidence interval for RP, —0.48 to —0.17), while the response in the control group showed no distinct pattern (RP = 0.17; 95% confidence interval for RP, —0.05 to 0.31). The difference between the groups was significant (P = .0002). The median change in patients was —26% (interquartile range, 37). Conclusions Pulsatile patellar blood flow in patellofemoral pain syndrome patients is markedly reduced when the knee is being flexed, which supports the previous notion of an ischemic mechanism involved in the pathogenesis of this pain syndrome.
Apoptosis is a natural stimulus of IL6R shedding and contributes to the proinflammatory trans-signaling function of neutrophils
Authors: Chalaris Athena , Rabe Björn , Paliga Krzysztof , Lange Hans , Laskay Tamas , Fielding Ceri A. , Jones Simon A. , Rose-John Stefan , Scheller Jürgen 
Published: June 2007

AbstractInterleukin 6 (IL6) trans-signaling has emerged as a prominent regulator of immune responses during both innate and acquired immunity. Regulation of IL6 trans-signaling is reliant upon the release of soluble IL6 receptor (sIL6R), which binds IL6 to create an agonistic IL6/sIL6R complex capable of activating cell types that would not normally respond to IL6 itself. Here we show that intrinsic and extrinsic apoptotic stimulation by DNA damage, cytokine deprivation, and Fas stimulation promotes shedding of sIL6R. Apoptosis-induced shedding of the IL6R was caspase dependent but PKC independent, with inhibition of ADAM17 preventing IL6R shedding. Such insight is relevant to the control of acute inflammation, where transition from the initial neutrophil infiltration to a more sustained population of mononuclear cells is essential for the resolution of the inflammatory process. This transitional event is governed by IL6 trans-signaling. This study demonstrates that IL6R is shed from apoptotic human neutrophils. In vivo studies in a murine inflammation model showed that neutrophil depletion resulted in reduced local sIL6R levels and a concomitant decrease in mononuclear cells, suggesting that apoptosis-induced IL6R shedding from neutrophils promotes IL6 trans-signaling and regulates the attraction of monocytic cells involved in the clearance of apoptotic neutrophils.
Polymorphisms and functional activity in superoxide dismutase and catalase genes in smokers with COPD
Authors: Mak J. C. W. , Ho S. P. , Yu W. C. , Choo K. L. , Chu C. M. , Yew W. W. , Lam W. K. , Chan-Yeung M. 
Published: June 2007

Increased oxidative stress has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). This study investigated the risk of COPD and the substitution of alanine 16 with valine (Ala16Val) polymorphism of manganese-superoxide dismutase (Mn-SOD) and the cytosine to thymidine transition of nucleotide -262 (-262C>T) polymorphism of the catalase gene, and the activity of erythrocyte SOD and catalase.The subjects were stable COPD patient ever smokers (n = 165) and healthy controls, matched for age and cigarette consumption. Genotyping of Mn-SOD at Ala16Val and the catalase gene at -262C>T was performed, and the functional activity of SOD and catalase in erythrocytes determined.There were no significant differences in the distribution of the different genotypes or allele frequencies between patients and controls for both the Mn-SOD and catalase genes. Among healthy controls or COPD patients, no differences were observed in erythrocyte SOD and catalase activity, irrespective of genotype. Significantly higher erythrocyte catalase activity was found in COPD patients than in healthy controls. The T/T catalase genotype and Ala/Ala Mn-SOD genotype were uncommon in the present Chinese population.The increase in erythrocyte catalase activity in Chinese patients with chronic obstructive pulmonary disease probably indicates dysfunction of the oxidant/antioxidant defence system, but it is unclear whether this increase is compensatory or a pathogenic factor.
A 10-year prospective surveillance ofMycobacterium tuberculosisdrug resistance in France 1995–2004
Authors: Khuê P. M. , Truffot-Pernot C. , Texier-Maugein J. , Jarlier V. , Robert J. 
Published: June 2007

Drug resistance surveillance and trend monitoring resistance rates bring some insights into tuberculosis (TB) control. The current study reports the characteristics of TB and drug resistance during a 10-yr prospective surveillance of culture-positive TB in France.Data for the current study was collected from 1995–2004viaa sentinel network of laboratories from university hospitals that complied with the international recommendations for the surveillance of drug resistance. Susceptibility test results were performed in each individual laboratory.Data on 13,283 patients were collected during the 10-yr period, 49% of whom had been born in France, 10% were HIV co-infected and 8% had previously been treated. As expected, previously treated and HIV co-infected patients were more likely to harbour resistant strains, especially rifampicin (RMP)-resistant strains. Among new patients, the mean resistance rate to at least one drug was 8.8%, and there was an upward trend in resistance to isoniazid and RMP (0.8–1%) related to the increase in the proportion of patients who had been born outside of France (38–53%). Among previously treated patients, the mean resistance rate to one drug was 20.6% and there was no significant time trend in resistance rates.The sentinel network provided valuable data on trends regarding the characteristics of tuberculosis and on drug resistance rates and reinforced the interest of analysing data by country of birth and history of treatment.
Early discharge of patients with pulmonary embolism: a two-phase observational study
Authors: Davies C. W. H. , Wimperis J. , Green E. S. , Pendry K. , Killen J. , Mehdi I. , Tiplady C. , Kesteven P. , Rose P. , Oldfield W. 
Published: June 2007

The aim of the present study was to assess whether patients with pulmonary embolism (PE) could be managed as outpatients after early discharge from hospital using low molecular weight heparin instead of remaining as in-patients until effective oral anticoagulation was achieved.Phase 1 of the study identified criteria for the safe discharge of selected patients; phase 2 treated a cohort of low-risk patients with PE as outpatients with tinzaparin using existing deep venous thrombosis services.In phase 1, 127 (56.4%) of 225 patients were considered unsuitable for outpatient management. Reasons included: admission for another medical reason; additional monitoring or requirement for oxygen; bleeding disorders; previous PE/further PE while on warfarin; co-existing major deep venous thrombosis; likelihood of poor compliance; significant immobility; and pregnancy. In phase 2, 157 patients with PE received outpatient anticoagulation therapy. There were no deaths, bleeding or recurrent thromboembolic events during acute treatment with low molecular weight heparin. The median (range) length of hospital stay was 1.0 (1–4) day, with a median saving of 5.0 (1–42) bed-days per patient.Patients were highly satisfied with outpatient management; 144 (96.6%) indicated that they would prefer treatment as outpatients for a subsequent pulmonary embolism. Early discharge and outpatient management of pulmonary embolism appears safe and acceptable in selected low-risk patients, and can be implemented using existing outpatient deep venous thrombosis services.
Use of tunnelled catheters for malignant pleural effusions in patients fit for pleurodesis
Authors: Tremblay A. , Mason C. , Michaud G. 
Published: June 2007

The aim of the present study was to examine the effectiveness of tunnelled pleural catheters (TPC) in patients with malignant pleural effusions who would otherwise be candidates for pleurodesis.Patients were selected from a previously reported database of 250 TPC insertions. The study group was selected based on lung re-expansion and survival as a surrogate maker of eligibility for pleurodesis procedure, as defined by survival of ≥90 days and lung re-expansion ≥80% post-drainage on a standard chest radiograph 2 weeks post TPC placement.There were 109 procedures in 97 patients that met the entry criteria. Spontaneous pleurodesis (SP) was achieved following 70% of procedures and correlated with symptom control. The mean time to SP was 90 days. There was no need for a repeat procedure in 87% of cases overall and in 92% of patients experiencing SP. There were few complications and no procedure-related deaths.Tunnelled pleural catheters are an effective way of controlling malignant pleural effusions when used as first-line treatment in patients who appear to be candidates for pleurodesis procedures.
Evaluation of sample size effect on the identification of haplotype blocks
Authors: Osabe Dai , Tanahashi Toshihito , Nomura Kyoko , Shinohara Shuichi , Nakamura Naoto , Yoshikawa Toshikazu , Shiota Hiroshi , Keshavarz Parvaneh , Yamaguchi Yuka , Kunika Kiyoshi , Moritani Maki , Inoue Hiroshi , Itakura Mitsuo 
Published: June 2007

Abstract

Background
Genome-wide maps of linkage disequilibrium (LD) and haplotypes have been created for different populations. Substantial sharing of the boundaries and haplotypes among populations was observed, but haplotype variations have also been reported across populations. Conflicting observations on the extent and distribution of haplotypes require careful examination. The mechanisms that shape haplotypes have not been fully explored, although the effect of sample size has been implicated. We present a close examination of the effect of sample size on haplotype blocks using an original computational simulation.

Results
A region spanning 19.31 Mb on chromosome 20q was genotyped for 1,147 SNPs in 725 Japanese subjects. One region of 445 kb exhibiting a single strong LD value (average |D'|; 0.94) was selected for the analysis of sample size effect on haplotype structure. Three different block definitions (recombination-based, LD-based, and diversity-based) were exploited to create simulations for block identification with θ value from real genotyping data. As a result, it was quite difficult to estimate a haplotype block for data with less than 200 samples. Attainment of a reliable haplotype structure with 50 samples was not possible, although the simulation was repeated 10,000 times.

Conclusion
These analyses underscored the difficulties of estimating haplotype blocks. To acquire a reliable result, it would be necessary to increase sample size more than 725 and to repeat the simulation 3,000 times. Even in one genomic region showing a high LD value, the haplotype block might be fragile. We emphasize the importance of applying careful confidence measures when using the estimated haplotype structure in biomedical research.
The Entamoeba histolytica genome: primary structure and expression of proteolytic enzymes
Authors: Tillack Manuela , Biller Laura , Irmer Henriette , Freitas Michelle , Gomes Maria A , Tannich Egbert , Bruchhaus Iris 
Published: June 2007

Abstract

Background
A number of studies have shown that peptidases and in particular cysteine peptidases constitute major pathogenicity factors in Entamoeba histolytica. Recent studies have suggested that a considerable number of genes coding for proteolytic enzymes are present within the E. histolytica genome and questions remain about the mode of expression of the various molecules.

Results
By homology search within the recently published amoeba genome, we identified a total of 86 E. histolytica genes coding for putative peptidases, including 46 recently described peptidase genes. In total these comprise (i) 50 cysteine peptidases of different families but most of which belong to the C1 papain superfamily, (ii) 22 different metallo peptidases from at least 11 different families, (iii) 10 serine peptidases belonging to 3 different families, and (iv) 4 aspartic peptidases of only one family. Using an oligonucleotide microarray, peptidase gene expression patterns of 7 different E. histolytica isolates as well as of heat stressed cells were analysed. A total of 21 out of 79 amoeba peptidase genes analysed were found to be significantly expressed under standard axenic culture conditions whereas the remaining are not expressed or at very low levels only. In heat-stressed cells the expression of 2 and 3 peptidase genes, respectively, were either decreased or increased. Only minor differences were observed between the various isolates investigated, despite the fact that these isolates were originated from asymptomatic individuals or from patients with various forms of amoebic diseases.

Conclusion

Entamoeba histolytica possesses a large number of genes coding for proteolytic enzymes. Under standard culture conditions or upon heat-stress only a relatively small number of these genes is significantly expressed and only very few variations become apparent between various clinical E. histolytica isolates, calling into question the importance of these enzymes in E. histolytica pathogenicity. Further studies are required to define the precise role of most of the proteolytic enzyme for amoeba cell biology but in particular for E. histolytica virulence.
A global view of Staphylococcus aureus whole genome expression upon internalization in human epithelial cells
Authors: Garzoni Christian , Francois Patrice , Huyghe Antoine , Couzinet Sabine , Tapparel Caroline , Charbonnier Yvan , Renzoni Adriana , Lucchini Sacha , Lew Daniel P , Vaudaux Pierre , Kelley William L , Schrenzel Jacques 
Published: June 2007

Abstract

Background

Staphylococcus aureus, a leading cause of chronic or acute infections, is traditionally considered an extracellular pathogen despite repeated reports of S. aureus internalization by a variety of non-myeloid cells in vitro. This property potentially contributes to bacterial persistence, protection from antibiotics and evasion of immune defenses. Mechanisms contributing to internalization have been partly elucidated, but bacterial processes triggered intracellularly are largely unknown.

Results
We have developed an in vitro model using human lung epithelial cells that shows intracellular bacterial persistence for up to 2 weeks. Using an original approach we successfully collected and amplified low amounts of bacterial RNA recovered from infected eukaryotic cells. Transcriptomic analysis using an oligoarray covering the whole S. aureus genome was performed at two post-internalization times and compared to gene expression of non-internalized bacteria. No signs of cellular death were observed after prolonged internalization of Staphylococcus aureus 6850 in epithelial cells. Following internalization, extensive alterations of bacterial gene expression were observed. Whereas major metabolic pathways including cell division, nutrient transport and regulatory processes were drastically down-regulated, numerous genes involved in iron scavenging and virulence were up-regulated. This initial adaptation was followed by a transcriptional increase in several metabolic functions. However, expression of several toxin genes known to affect host cell integrity appeared strictly limited.

Conclusion
These molecular insights correlated with phenotypic observations and demonstrated that S. aureus modulates gene expression at early times post infection to promote survival. Staphylococcus aureus appears adapted to intracellular survival in non-phagocytic cells.
Functional distribution of Ca2+-coupled P2 purinergic receptors among adrenergic and noradrenergic bovine adrenal chromaffin cells
Authors: Tomé Ângelo R , Castro Enrique , Santos Rosa M , Rosário Luís M 
Published: June 2007

AbstractBackgroundAdrenal chromaffin cells mediate acute responses to stress through the release of epinephrine. Chromaffin cell function is regulated by several receptors, present both in adrenergic (AD) and noradrenergic (NA) cells. Extracellular ATP exerts excitatory and inhibitory actions on chromaffin cells via ionotropic (P2X) and metabotropic (P2Y) receptors. We have taken advantage of the actions of the purinergic agonists ATP and UTP on cytosolic free Ca2+concentration ([Ca2+]i) to determine whether P2X and P2Y receptors might be asymmetrically distributed among AD and NA chromaffin cells.ResultsThe [Ca2+]iand the [Na+]iwere recorded from immunolabeled bovine chromaffin cells by single-cell fluorescence imaging. Among the ATP-sensitive cells ~40% did not yield [Ca2+]iresponses to ATP in the absence of extracellular Ca2+(Ca2+o), indicating that they expressed P2X receptors and did not express Ca2+- mobilizing P2Y receptors; the remainder expressed Ca2+-mobilizing P2Y receptors. Relative to AD-cells approximately twice as many NA-cells expressed P2X receptors while not expressing Ca2+- mobilizing P2Y receptors, as indicated by the proportion of cells lacking [Ca2+]iresponses and exhibiting [Na+]iresponses to ATP in the absence and presence of Ca2+o, respectively. The density of P2X receptors in NA-cells appeared to be 30–50% larger, as suggested by comparing the average size of the [Na+]iand [Ca2+]iresponses to ATP. Conversely, approximately twice as many AD-cells expressed Ca2+-mobilizing P2Y receptors, and they appeared to exhibit a higher (~20%) receptor density. UTP raised the [Ca2+]iin a fraction of the cells and did not raise the [Na+]iin any of the cells tested, confirming its specificity as a P2Y agonist. The cell density of UTP-sensitive P2Y receptors did not appear to vary among AD- and NA-cells.ConclusionAlthough neither of the major purinoceptor types can be ascribed to a particular cell phenotype, P2X and Ca2+-mobilizing P2Y receptors are preferentially located to noradrenergic and adrenergic chromaffin cells, respectively. ATP might, in addition to an UTP-sensitive P2Y receptor, activate an UTP-insensitive P2Y receptor subtype. A model for a short-loop feedback interaction is presented whereby locally released ATP acts upon P2Y receptors in adrenergic cells, inhibiting Ca2+influx and contributing to terminate evoked epinephrine secretion.