bluuebunny/crossref_metadata_2025_split huggingface dataset:
How Does Chronic Sildenafil Prevent Vascular Oxidative Stress in Insulin-Resistant Rats?
Authors: Oudot Alexandra , Behr-Roussel Delphine , Le Coz Olivier , Poirier Sarah , Bernabe Jacques , Alexandre Laurent , Giuliano François 
Published: October 2009

ABSTRACT

Introduction
Insulin resistance features both endothelial dysfunction and increased oxidative stress. Both disorders are targeted by a chronic treatment with sildenafil. However, the mechanism of action by which chronic sildenafil exerts its effects on reactive oxygen species sources is still largely unknown.

Aim
We therefore investigated how chronic sildenafil administration could impact vascular endothelial NO and superoxide release in a rat model of insulin resistance induced by fructose overload.

Methods
Adult male Wistar rats were fed a fructose-enriched diet (fructose-fed rats [FFR]) for 9 weeks. From weeks 6–8, sildenafil was administered subcutaneously twice daily (20 mg/kg), followed by a 1-week washout.

Main Outcome Measures
Vascular endothelial NO and superoxide release were monitored in vitro in thoracic aortic segments using oxidative fluorescence. Specific inhibitors were used to distinguish the respective role of the main superoxide-producing systems within the vascular wall (i.e., mitochondrial respiratory chain and NADPH oxidases). The levels of expression of eNOS, Akt, and NADPH oxidase subunits were determined in the abdominal aorta.

Results
Chronic sildenafil administration corrected hyperglycemia, hyperinsulinemia, and hypertriglyceridemia in FFR. Moreover, after 9 weeks of diet, while global unstimulated aortic endothelial NO and superoxide release were unchanged in FFR, the relative contribution of the mitochondrial respiratory chain and NADPH oxidases was modified. Chronic sildenafil treatment, even after the 1-week washout period, was able to increase endothelial NO release independently of Akt-dependent phosphorylation by up-regulating eNOS expression, and restored the relative contribution of each superoxide-producing system examined, yielding endothelial superoxide release. Finally, in vitro incubation of aortic segments with sildenafil markedly decreased the endothelial aortic superoxide release.

Conclusions
The present study showed that chronic sildenafil produced sustained vascular antioxidant effects in insulin-resistant rats by increasing NO release and regulating vascular superoxide release, supporting therefore further investigations using chronic sildenafil administration in preventing cardiovascular alterations associated with oxidative stress.
Differential indirect effects of two plant viruses on an invasive and an indigenous whitefly vector: implications for competitive displacement
Authors: Liu J. , Zhao H. , Jiang K. , Zhou X.‐P. , Liu S.‐S. 
Published: October 2009

AbstractThe role of vector–begomovirus–plant interactions in the widespread invasion by some members of the whitefly species complex Bemisia tabaci is poorly understood. The invasive B biotype of B. tabaci entered China in the late 1990s and had become the predominant or only biotype of the whitefly in many regions of the country by 2005–2006. Meanwhile epidemics of begomoviruses have been observed in many crops including tomato for which Tomato yellow leaf curl China virus (TYLCCNV) and Tomato yellow leaf curl virus (TYLCV) have been identified as two major disease‐causing agents. Here, we conducted laboratory experiments to compare the performance of the invasive B and indigenous ZHJ1 whitefly biotypes on uninfected, TYLCCNV‐infected and TYLCV‐infected plants of tomato cv. Hezuo903, a cultivar that has been widely cultivated in many regions of China. The infection of tomato plants by either of the viruses had no or only marginal effects on the development, survival and fecundity of the B biotype. In contrast, survival and fecundity of the ZHJ1 biotype were significantly reduced on virus‐infected plants compared to those on uninfected plants. Populations of the B biotype on uninfected and TYLCCNV‐infected plants increased at similar rates, whereas population increase of the ZHJ1 biotype on TYLCCNV‐infected plants was affected adversely. These asymmetric responses to virus infection of tomato plants between the B and ZHJ1 biotypes are likely to offer advantages to the B biotype in its invasion and displacement of the indigenous biotype.
Effectiveness of canalicular laceration repair using monocanalicular intubation with Monoka tubes
Authors: Lee Hwa , Chi Mijung , Park Minsoo , Baek Sehyun 
Published: October 2009

Abstract.Purpose:  This study aimed to evaluate the clinical efficacy of canalicular laceration repair using monocanalicular intubation with Monoka tubes.Methods:  A total of 36 single lacerated canaliculi were repaired using monocanalicular intubation with Monoka tubes, without mucosal anastomosis of the canaliculi, and were retrospectively reviewed. Demographic information, injury locations, associated ocular injuries, complications and outcomes were analysed.Results:  Mean patient age was 34 years (range 1–64 years). Tubes were removed at a mean of 4.2 months (range 3–6 months). There were 26 lower canalicular lacerations (72%) and 10 upper canalicular lacerations (28%). Overall, 34 of 36 cases (92%) showed improvement in symptoms and exhibited positivity on the dye disappearance test at 4–12 months after the procedure (mean 7.8 months). In total, 21 patients (58%) achieved complete success, 13 patients (36%) achieved partial success and two patients (6%) suffered surgical failure. Complications were seen in five cases and included two early tube protrusions, two punctal slits and one punctal granuloma.Conclusions:  Monocanalicular intubation with Monoka tubes leads to successful outcomes without significant complications and offers an alternative to bicanalicular intubation in the treatment of monocanalicular lacerations.
Intraocular pressure in keratoconus
Authors: Read Scott A. , Collins Michael J. 
Published: October 2009

Abstract.Purpose:  This study aimed to investigate intraocular pressure (IOP) measurements taken using the dynamic contour tonometer (DCT) and the non‐contact tonometer (NCT) in subjects with keratoconus.Methods:  Intraocular pressure was measured in 20 keratoconus subjects and 20 age‐matched control subjects using the DCT and NCT instruments. Central and off‐centre measures were taken with the DCT in order to highlight any systematic errors associated with corneal biomechanical factors. Measures of anterior and posterior corneal topography and thickness were also taken in each subject.Results:  No significant difference was found between the central and off‐centre DCT IOP readings for the keratoconus subjects and age‐matched controls (p > 0.05). The average DCT IOP was 14.2 ± 1.4 mmHg in the keratoconus subjects and 14.2 ± 1.6 mmHg in the controls. However, the average NCT readings differed significantly (p < 0.001) between the keratoconus subjects (9.2 ± 1.5 mmHg) and the controls (12.9 ± 2.4 mmHg). Intraocular pressure measurements taken with the DCT showed no significant (p > 0.05) correlation with the severity of keratoconus as determined through measures of corneal topography and thickness. Equivalent IOP measurements taken with the NCT correlated significantly with certain measures of corneal curvature and thickness in the keratoconus population. The difference between DCT and NCT IOP was strongly correlated with measures of corneal topography and thickness, with differences increasing in more advanced keratoconus.Conclusions:  The measurements obtained with the DCT do not appear to be dependent upon corneal factors, unlike those taken with the NCT. The presence or severity of keratoconus was not correlated with DCT IOP values.
Globalizing Justice: The Contribution of Christian Spirituality
Authors: Groody Daniel G. 
Published: October 2009

AbstractThis article looks at the role of Christian spirituality in fostering right relationships. It looks first at the integral relationship between spirituality and justice, particularly as it takes shape within the terrain of the human heart. Secondly, it examines the role of social context in a transformative spirituality by looking at one faith community of undocumented immigrants in the United States. And thirdly it looks at migration as a metaphor for a spirituality of transformation, one that orients a pilgrim people towards a homeward journey and awakens in us a social conscience. The central argument is that spiritual transformation is about the movement towards authenticity, where the gift of peace grows from the rebuilding of our relationships with God, ourselves and others.
Patients with Long-Term Oral Carriage Harbor High-Persister Mutants of
Candida albicans
Authors: LaFleur Michael D. , Qi Qingguo , Lewis Kim 
Published: October 2009

ABSTRACT

Fungal biofilms produce a small number of persister cells which can tolerate high concentrations of fungicidal agents. Persisters form upon attachment to a surface, an important step in the pathogenesis of
Candida
strains. The periodic application of antimicrobial agents may select for strains with increased levels of persister cells. In order to test this possibility, 150 isolates of
Candida albicans
and
C. glabrata
were obtained from cancer patients who were at high risk for the development of oral candidiasis and who had been treated with topical chlorhexidine once a day. Persister levels were measured by exposing biofilms growing in the wells of microtiter plates to high concentrations of amphotericin B and plating for survivors. The persister levels of the isolates varied from 0.2 to 9%, and strains isolated from patients with long-term carriage had high levels of persisters. High-persister strains were isolated from every patient with
Candida
carriage of more than 8 consecutive weeks but from no patients with transient carriage. All of the high-persister isolates had an amphotericin B MIC that was the same as that for the wild type, indicating that these strains were drug-tolerant rather than drug-resistant mutants. Biofilms of the majority of high-persister strains also showed an increased tolerance to chlorhexidine and had the same MIC for this antimicrobial as the wild type. This study suggests that persister cells are clinically relevant, and antimicrobial therapy selects for high-persister strains in vivo. The drug tolerance of persisters may be a critical but overlooked component responsible for antimicrobial drug failure and relapsing infections.
Continuous Clindamycin Infusion, an Innovative Approach to Treating Bone and Joint Infections
Authors: Zeller Valérie , Dzeing-Ella Arnaud , Kitzis Marie-Dominique , Ziza Jean-Marc , Mamoudy Patrick , Desplaces Nicole 
Published: October 2009

ABSTRACT

The feasibility, safety, and efficacy of prolonged, continuous, intravenous clindamycin therapy were retrospectively evaluated for 70 patients treated for bone and joint infections, 40% of whom were treated as outpatients. The median treatment duration was 40 days, the median daily clindamycin dose was 2,400 mg, and three moderate-grade adverse events occurred. The median serum clindamycin concentrations on days 3 to 14 and days 8 to 28 were 5 and 6.2 mg/liter, respectively; the median concentration was significantly lower (
P
< 0.02) in patients treated with rifampin (5.3 mg/liter) than in those not treated with rifampin (8.9 mg/liter). Among 53 patients with a median follow-up of 30 months (range, 24 to 53 months), 49 (92%) were considered cured (1 patient had a relapse, and 3 patients had reinfections).
In Vitro Activity of Mirincamycin (U24729A) against
Plasmodium falciparum
Isolates from Gabon
Authors: Held Jana , Westerman Richard , Kremsner Peter G. , Mordmüller Benjamin 
Published: October 2009

ABSTRACT

We assessed the in vitro activity of mirincamycin, a lincosamide antibiotic, against
Plasmodium falciparum
clinical isolates from Gabon. Growth was determined by HRP2 enzyme-linked immunosorbent assay using an adapted protocol with a prolonged incubation time (6 days) to account for antibiotic-induced delayed death. Mirincamycin's
cis
and
trans
isomers are more active (median 50% inhibitory concentrations [IC
50
s], 3.2 nM and 2.6 nM) than the comparator drugs clindamycin (IC
50
, 12 nM) and doxycycline (IC
50
, 720 nM), and therefore, further clinical development is promising.
Mouse Macrophages Are Permissive to MotileLegionellaSpecies That Fail To Trigger Pyroptosis
Authors: Whitfield Natalie N. , Byrne Brenda G. , Swanson Michele S. 
Published: October 2009

ABSTRACTLegionella pneumophila, a motile opportunistic pathogen of humans, is restricted from replicating in the lungs of C57BL/6 mice. Resistance of mouse macrophages toL. pneumophiladepends on recognition of cytosolic flagellin. Once detected by the NOD-like receptors Naip5 and Ipaf (Nlrc4), flagellin triggers pyroptosis, a proinflammatory cell death. In contrast, motile strains ofL. parisiensisandL. tucsonensisreplicate profusely within C57BL/6 macrophages, similar to flagellin-deficientL. pneumophila. To gain insight into how motile species escape innate defense mechanisms of mice, we compared their impacts on macrophages.L. parisiensisandL. tucsonensisdo not induce proinflammatory cell death, as measured by lactate dehydrogenase (LDH) release and interleukin-1β (IL-1β) secretion. However, flagellin isolated fromL. parisiensisandL. tucsonensistriggers cell death and IL-1β secretion when transfected into the cytosol of macrophages. Neither strain displays three characteristics of the canonicalL. pneumophilaDot/Icm type IV secretion system: sodium sensitivity, LAMP-1 evasion, and pore formation. Therefore, we postulate that whenL. parisiensisandL. tucsonensisinvade a mouse macrophage, flagellin is confined to the phagosome, protecting the bacteria from recognition by the cytosolic surveillance system and allowingLegionellato replicate. Despite their superior capacity to multiply in mouse macrophages,L. parisiensisandL. tucsonensishave been associated with only two cases of disease, both in renal transplant patients. These results point to the complexity of disease, a product of the pathogenic potential of the microbe, as defined in the laboratory, and the capacity of the host to mount a measured defense.
Mannose Receptor-Dependent Delay in Phagosome Maturation by
Mycobacterium avium
Glycopeptidolipids
Authors: Sweet Lindsay , Singh Prachi P. , Azad Abul K. , Rajaram Murugesan V. S. , Schlesinger Larry S. , Schorey Jeffrey S. 
Published: October 2009

ABSTRACT

The ability of pathogenic mycobacteria to block phagosome-lysosome fusion is critical for its pathogenesis. The molecules expressed by mycobacteria that inhibit phagosome maturation and the mechanism of this inhibition have been extensively studied. Recent work has indicated that mannosylated lipoarabinomannan (ManLAM) isolated from
Mycobacterium tuberculosis
can function to delay phagosome-lysosome fusion and that this delay requires the interaction of ManLAM with the mannose receptor (MR). However, the molecules expressed by other pathogenic mycobacteria that function to inhibit phagosome maturation have not been well described. In the present study, we show that phagosomes containing silica beads coated with glycopeptidolipids (GPLs), a major surface component of
Mycobacterium avium
, showed limited acidification and delayed recruitment of late endosomal/lysosomal markers compared to those of phosphatidylcholine-coated beads. The carbohydrate component of the GPLs was required, as beads coated only with the lipopeptide core failed to delay phagosome-lysosome fusion. Moreover, the ability of GPLs to delay phagosome maturation was dependent on the macrophage expression of the MR. Using CHO cells expressing the MR, we confirmed that the GPLs bind this receptor. Finally, human monocyte-derived macrophages knocked down for MR expression showed increased
M. avium
phagosome-lysosome fusion relative to control cells. Together, the data indicate that GPLs can function to delay phagosome-lysosome fusion and suggest that GPLs, like ManLAM, work through the MR to mediate this activity.
Characterization of Novel β-Galactosidase Activity That Contributes to Glycoprotein Degradation and Virulence in
Streptococcus pneumoniae
Authors: Terra Vanessa S. , Homer Karen A. , Rao Susmitha G. , Andrew Peter W. , Yesilkaya Hasan 
Published: October 2009

ABSTRACT

The pneumococcus obtains its energy from the metabolism of host glycosides. Therefore, efficient degradation of host glycoproteins is integral to pneumococcal virulence. In search of novel pneumococcal glycosidases, we characterized the
Streptococcus pneumoniae
strain D39 protein encoded by
SPD_0065
and found that this gene encodes a β-galactosidase. The SPD_0065 recombinant protein released galactose from desialylated fetuin, which was used here as a model of glycoproteins found
in vivo
. A pneumococcal mutant with a mutation in
SPD_0065
showed diminished β-galactosidase activity, exhibited an extended lag period in mucin-containing defined medium, and cleaved significantly less galactose than the parental strain during growth on mucin. As pneumococcal β-galactosidase activity had been previously attributed solely to
SPD_0562
(
bgaA
), we evaluated the contribution of
SPD_0065
and
SPD_0562
to total β-galactosidase activity. Mutation of either gene significantly reduced enzymatic activity, but β-galactosidase activity in the double mutant, although significantly less than that in either of the single mutants, was not completely abolished. The expression of
SPD_0065
in
S. pneumoniae
grown in mucin-containing medium or tissues harvested from infected animals was significantly upregulated compared to that in pneumococci from glucose-containing medium. The
SPD_0065
mutant strain was found to be attenuated in virulence in a manner specific to the host tissue.
The Presence of CD14 Overcomes Evasion of Innate Immune Responses by VirulentFrancisella tularensisin Human Dendritic Cells In Vitro and Pulmonary Cells In Vivo
Authors: Chase Jennifer C. , Bosio Catharine M. 
Published: October 2009

ABSTRACTFrancisella tularensisis a Gram-negative bacterium that causes acute, lethal disease following inhalation. We have previously shown that viableF.tularensisfails to stimulate secretion of proinflammatory cytokines following infection of human dendritic cells (hDC) in vitro and pulmonary cells in vivo. Here we demonstrate that the presence of the CD14 receptor is critical for detection of virulentF.tularensisstrain SchuS4 by dendritic cells, monocytes, and pulmonary cells. Addition of soluble CD14 (sCD14) to hDC restored cytokine production following infection with strain SchuS4. In contrast, addition of anti-CD14 to monocyte cultures inhibited the ability of these cells to respond to strain SchuS4. Addition of CD14 or blocking CD14 following SchuS4 infection in dendritic cells and monocytes, respectively, was not due to alterations in phagocytosis or replication of the bacterium in these cells. Administration of sCD14 in vivo also restored cytokine production following infection with strain SchuS4, as assessed by increased concentrations of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-12p70, and IL-6 in the lungs of mice receiving sCD14 compared to mock-treated controls. In contrast to homogenous cultures of monocytes or dendritic cells infected in vitro, mice treated with sCD14 in vivo also exhibited controlled bacterial replication and dissemination compared to mock-treated controls. Interestingly, animals that lacked CD14 were not more susceptible or resistant to pulmonary infection with SchuS4. Together, these data support the hypothesis that the absence or low abundance of CD14 on hDC and in the lung contributes to evasion of innate immunity by virulentF.tularensis. However, CD14 is not required for development of inflammation during the last 24 to 48 h of SchuS4 infection. Thus, the presence of this receptor may aid in control of virulentF.tularensisinfections at early, but not late, stages of infection.
Helicobacter pylori
Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses
Authors: Kido Masahiro , Tanaka Junya , Aoki Nobuhiro , Iwamoto Satoru , Nishiura Hisayo , Chiba Tsutomu , Watanabe Norihiko 
Published: October 2009

ABSTRACT

Helicobacter pylori
colonizes the stomach and induces strong, specific local and systemic humoral and cell-mediated immunity, resulting in the development of chronic gastritis in humans. Although
H. pylori
-induced chronic atrophic gastritis is characterized by marked infiltration of T helper type 1 (Th1) cytokine-producing CD4
+
T cells, almost all of the inflamed gastric mucosae also contain focal lymphoid aggregates with germinal centers. In addition, typical
H. pylori
-induced chronic gastritis in children, called follicular gastritis, is characterized by B-cell follicle formation in the gastric mucosa. The aim of this study was to examine whether thymic stromal lymphopoietin (TSLP), an epithelial-cell-derived cytokine inducing a dendritic cell (DC)-mediated inflammatory Th2 response, is involved in Th2 responses triggering B-cell activation in
H. pylori
-induced gastritis. Here, we show that
H. pylori
triggered human gastric epithelial cells to produce TSLP, together with the DC-attracting chemokine MIP-3α and the B-cell-activating factor BAFF. After DCs were incubated with supernatants from
H. pylori
-infected epithelial cells, the conditioned cells expressed high levels of costimulatory molecules, such as CD80, and triggered naïve CD4
+
T cells to produce high levels of the Th2 cytokines interleukin-4 and interleukin-13 and of the inflammatory cytokines tumor necrosis factor alpha and gamma interferon. In contrast, after incubation of the supernatants with the neutralizing antibodies to TSLP, the conditioned DCs did not prime T cells to produce high levels of Th2 cytokines. These results, together with the finding that TSLP was expressed by the epithelial cells of human follicular gastritis, suggest that
H. pylori
can directly trigger epithelial cells to produce TSLP. It also suggests that TSLP-mediated DC activation may be involved in Th2 responses triggering B-cell activation in
H. pylori
-induced gastritis.
Host Chemokine and Cytokine Response in the Endocervix within the First Developmental Cycle of
Chlamydia muridarum
Authors: Rank Roger G. , Lacy H. Marie , Goodwin Anna , Sikes James , Whittimore Judy , Wyrick Priscilla B. , Nagarajan Uma M. 
Published: October 2009

ABSTRACT

The initial host response in a primary chlamydial infection is the onset of acute inflammation. However, we still know very little about the early temporal events in the induction of the acute inflammatory response and how these events relate to the initial chlamydial developmental cycle in an actual genital infection. Because it was critical to initiate a synchronous infection in the endocervix in the first 24 h to evaluate the sequential expression of the host response, we developed the surgical methodology of depositing
Chlamydia muridarum
directly on the endocervix. Cervical tissue was collected at 3, 12, and 24 h after inoculation and the expression array of chemokines, cytokines, and receptors was assessed to characterize the response during the initial developmental cycle. Polymorphonuclear leukocyte (PMN) infiltration was first observed at 12 h after inoculation, and a few PMNs could be seen in the epithelium at 24 h. Electron microscopic analysis at 24 h showed that virtually all inclusions were at the same stage of development, indicating a synchronous infection. Several chemokine and cytokine genes were expressed as early as 3 h after infection, but by 12 h, 41 genes were expressed. Thus, activation of the host response occurs both with the introduction of elementary bodies into the host and early replication of reticulate bodies. No significant response was observed when UV-inactivated organisms were inoculated into the cervix at any time interval. This model provides an ideal opportunity to investigate the mechanisms by which the early inflammatory response is induced in vivo.