bluuebunny/crossref_metadata_2025_split huggingface dataset:
Binding of Excreted and/or Secreted Products of Adult Hookworms to Human NK Cells inNecator americanus-Infected Individuals from Brazil
Authors: Teixeira-Carvalho Andréa , Fujiwara Ricardo T. , Stemmy Erik J. , Olive Denise , Damsker Jesse M. , Loukas Alex , Corrêa-Oliveira Rodrigo , Constant Stephanie L. , Bethony Jeffrey M. 
Published: October 2008

ABSTRACTThe impact of the interaction between excreted and/or secreted (ES)Necator americanusproducts and NK cells fromNecator-infected individuals was analyzed. We investigated the binding of ES products to NK cells, the expression of NK cell receptors (CD56, CD159a/NKG2A, CD314/NKG2D, CD335/NKp46, and KLRF1/NKp80), the frequency of gamma interferon (IFN-γ)-producing NK cells after whole-blood in vitro stimulation, and the capacity ofN. americanusES products to induce NK cell chemotaxis. In contrast to those from noninfected individuals, NK cells fromNecator-infected individuals demonstrated no binding withN. americanusES products. This phenomenon was not due to alterations in NK cell receptor expression in infected subjects and could not be reproduced with NK cells from uninfected individuals by incubation with immunoregulatory cytokines (interleukin-10/transforming growth factor β). Further, we found that a significantly greater percentage of NK cells from infected subjects than NK cells from uninfected individuals spontaneously produced IFN-γ upon ex vivo culture. Our findings support a model whereby NK cells fromNecator-infected individuals may interact with ES products, making these cells refractory to binding with exogenous ES products. DuringN. americanusinfection, human NK cells are attracted to the site of infection by chemotactic ES products produced by adultNecatorworms in the gut mucosa. Binding of ES products causes the NK cells to become activated and secrete IFN-γ locally, thereby contributing to the adult hookworm's ability to evade host immune responses.
Uropathogenic
Escherichia coli
CFT073 Is Adapted to Acetatogenic Growth but Does Not Require Acetate during Murine Urinary Tract Infection
Authors: Anfora Andrew T. , Halladin David K. , Haugen Brian J. , Welch Rodney A. 
Published: October 2008

ABSTRACT

In vivo accumulation of
d
-serine by
Escherichia coli
CFT073 leads to elevated expression of PAP fimbriae and hemolysin by an unknown mechanism. Loss of
d
-serine catabolism by CFT073 leads to a competitive advantage during murine urinary tract infection (UTI), but loss of both
d
- and
l
-serine catabolism results in attenuation. Serine is the first amino acid to be consumed in closed tryptone broth cultures and precedes the production of acetyl phosphate, a high-energy molecule involved in intracellular signaling, and the eventual secretion of acetate. We propose that the colonization defect associated with the loss of serine catabolism is due to perturbations of acetate metabolism. CFT073 grows more rapidly on acetogenic substrates than does
E. coli
K-12 isolate MG1655. As shown by transcription microarray results,
d
-serine is catabolized into acetate via the phosphotransacetylase (
pta
) and acetate kinase (
ackA
) genes while downregulating expression of acetyl coenzyme A synthase (
acs
). CFT073
acs
, which is unable to reclaim secreted acetate, colonized mouse bladders and kidneys in the murine model of UTI indistinguishably from the wild type. Both
pta
and
ackA
are involved in the maintenance of intracellular acetyl phosphate. CFT073
pta
and
ackA
mutants were screened to investigate the role of acetyl phosphate in UTI pathogenesis. Both single mutants are at a competitive disadvantage relative to the wild type in the kidneys but normally colonize the bladder. CFT073
ackA pta
was attenuated in both the bladder and the kidneys. Thus, we demonstrate that CFT073 is adapted to acetate metabolism as a result of requiring a proper cycling of the acetyl phosphate pathway for colonization of the upper urinary tract.
Implications of bevacizumab on vascular endothelial growth factor and endostatin in human choroidal neovascularisation
Authors: Tatar O , Shinoda K , Kaiserling E , Claes C , Eckardt C , Eckert T , Pertile G , Boeyden V , Scharioth G B , Yoeruek E , Szurman P , Bartz-Schmidt K U , Group Tuebingen Bevacizumab Study , Grisanti S 
Published: October 2008

Aim:To evaluate the implications of intravitreal bevacizumab on proangiogenic vascular endothelial growth factor (VEGF) with regard to the endogenous angiogenesis inhibitor endostatin in human choroidal neovascularisation (CNV) secondary to age-related macular degeneration.Methods:Retrospective review of an interventional case series of 48 patients who underwent full macular translocation surgery with removal of CNV. Twenty-five patients were treated with intravitreal bevacizumab injection 1 to 154 days prior to surgery (bevacizumab CNV). Twenty-three CNV without any kind of previous treatment were used as controls (control CNV). CNV were stained for CD34, cytokeratin18, VEGF, endostatin and E-selectin. A “predominance score of VEGF over endostatin” (PS) was defined by the difference between VEGF and endostatin staining scores.Results:Bevacizumab CNV revealed a weaker VEGF expression in endothelial cells (p = 0.0245) but significantly more intense endostatin in retina pigment epithelium (RPE) (p = 0.0001) and stroma (p<0.0001). Consequently, PS was significantly lower in RPE (p = 0.02), vessels (p = 0.03) and stroma (p = 0.0004) in bevacizumab CNV. The intensity of E-selectin expression in bevacizumab CNV was comparable with that in control CNV.Conclusions:A shift within the angiogenic balance in terms of decreased VEGF predominance over endostatin is detected in human CNV treated with bevacizumab.
One-year follow-up of a randomised controlled trial on added splinting to eccentric exercises in chronic midportion Achilles tendinopathy
Authors: de Jonge S , de Vos R J , Van Schie H T M , Verhaar J A N , Weir A , Tol J L 
Published: October 2008

ObjectiveThe study examined whether the addition of a night splint to eccentric exercises is beneficial for functional outcome in chronic midportion Achilles tendinopathy.DesignOne-year follow-up of a randomised controlled single blinded clinical trial.SettingSports medicine department in a general hospital.Patients58 patients (70 tendons) were included.InterventionsAll patients completed a 12-week heavy load eccentric training programme. One group received a night splint in addition to eccentric exercises.Main outcome measurementsOutcome scores were: Victorian Institute of Sport Assessment—Achilles (VISAA) score, subjective patient satisfaction and neovascularisation score measured with power Doppler ultrasonography (PDU).ResultsFor both groups the VISA-A score increased significantly (from 50 to 76 (p<0.01) in the eccentric group and from 49 to 78 (p<0.01) in the night splint group). No significant differences in the VISA-A score were found between the groups from baseline to one year (p = 0.32). The presence of neovessels at baseline did not predict a change in the VISA-A score after one year in the whole group (p = 0.71).ConclusionEccentric exercises with or without a night splint improved functional outcome at one year follow-up. At follow-up there was no significant difference in clinical outcome when a night splint was used in addition to an eccentric exercise programme. Between 3 months and one year follow-up, a continuing increase in the VISA-A score was found. Assessment of the neovascularisation score with PDU at baseline has no prognostic value on long-term clinical outcome.
Altered hip and trunk muscle function in individuals with patellofemoral pain
Authors: Cowan S M , Crossley K M , Bennell K L 
Published: October 2008

Objective:The purpose of this study was to investigate the role of hip muscles in patellofemoral pain (PFP), specifically by investigating neuromotor control, strength and range of motion of the hip muscles.Design:Cross-sectional.Setting:University laboratory.Patients:Ten participants diagnosed with PFP and 27 asymptomatic controls were recruited, using standard inclusion and exclusion criteria.Main outcome measures:Electromyographic activity of the vasti and anterior gluteus medius (GM) were recorded using surface electrodes and posterior GM using fine wire electrodes while the participant completed a stair-stepping task. Hip strength and trunk side flexion strength was assessed using a hand-held dynamometer and hip range of motion with an inclinometer. Pain and disability measures were recorded for the PFP participants.Results:When individuals with PFP completed the stair-stepping task there was a delay in activation of both anterior and posterior GM (p<0.02) and an alteration in vasti control (p = 0.001). In addition, trunk side flexion strength was significantly less (29%) in individuals with PFP (p = 0.03).Conclusion:This study provides evidence that trunk side flexion strength and neuromotor control of the GM are affected in people with PFP. This study also confirms the presence of a delayed vastus medialis obliquus relative to vastus lateralis, providing further evidence underpinning the importance of retraining the vasti function in patients with PFP.
Partitioning of myelin basic protein into membrane microdomains in a spontaneously demyelinating mouse model for multiple sclerosisThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB — Membrane Proteins in Health and Disease.
Authors: DeBruin Lillian S. , Haines Jeffery D. , Bienzle Dorothee , Harauz George 
Published: October 2008

We have characterized the lipid rafts in myelin from a spontaneously demyelinating mouse line (ND4), and from control mice (CD1 background), as a function of age and severity of disease. Myelin was isolated from the brains of CD1 and ND4 mice at various ages, and cold lysed with 1.5% CHAPS (3-[(3-cholamidopropyl) dimethylammonio]-1-propanesulphonate). The lysate was separated by low-speed centrifugation into supernatant and pellet fractions, which were characterized by Western blotting for myelin basic protein (MBP) isoforms and their post-translationally modified variants. We found that, with maturation and with disease progression, there was a specific redistribution of the 14–21.5 kDa MBP isoforms (classic exon-II-containing vs exon-II-lacking) and phosphorylated forms into the supernatant and pellet. Further fractionation of the supernatant to yield detergent-resistant membranes (DRMs), representing coalesced lipid rafts, showed these to be highly enriched in exon-II-lacking MBP isoforms, and deficient in methylated MBP variants, in mice of both genotypes. The DRMs from the ND4 mice appeared to be enriched in MBP phosphorylated by MAP kinase at Thr95 (murine 18.5 kDa numbering). These studies indicate that different splice isoforms and post-translationally modified charge variants of MBP are targeted to different microdomains in the myelin membrane, implying multifunctionality of this protein family in myelin maintenance.
K–Cl cotransport in red blood cells from patients with KCC3 isoform mutantsThis paper is one of a selection of papers published in this Special Issue, entitled CSBMCB — Membrane Proteins in Health and Disease.
Authors: Lauf P.K. , Adragna N.C. , Dupre N. , Bouchard J.P. , Rouleau G.A. 
Published: October 2008

Red blood cells (RBCs) possess the K–Cl cotransport (KCC) isoforms 1, 3, and 4. Mutations within a given isoform may affect overall KCC activity. In a double-blind study, we analyzed, with Rb as a K congener, K fluxes (total flux, ouabain-sensitive Na+/K+ pump, and bumetanide-sensitive Na–K–2Cl cotransport, Cl-dependent, and ouabain- and bumetanide-insensitive KCC with or without stimulation by N-ethylmaleimide (NEM) and staurosporine or Mg removal, and basal channel-mediated fluxes, osmotic fragility, and ions and water in the RBCs of 8 controls, and of 8 patients with hereditary motor and sensory neuropathy with agenesis of corpus callosum (HMSN–ACC) with defined KCC3 mutations (813FsX813 and Phe529FsX532) involving the truncations of 338 and 619 C-terminal amino acids, respectively. Water and ion content and, with one exception, mean osmotic fragility, as well as K fluxes without stimulating agents, were similar in controls and HMSN–ACC RBCs. However, the NEM-stimulated KCC was reduced 5-fold (p < 0.0005) in HMSN–ACC vs control RBCs, as a result of a lower Vmax (p < 0.05) rather than a lower Km (p = 0.109), accompanied by corresponding differences in Cl activation. Low intracellular Mg activated KCC in 6 out of 7 controls vs 1 out of 6 HMSN–ACC RBCs, suggesting that regulation is compromised. The lack of differences in staurosporine-activated KCC indicates different action mechanisms. Thus, in HMSN–ACC patients with KCC3 mutants, RBC KCC activity, although indistinguishable from that of the control group, responded differently to biochemical stressors, such as thiol alkylation or Mg removal, thereby indirectly indicating an important contribution of KCC3 to overall KCC function and regulation.
Inhibition of heme oxygenase activity in newborn mice by azalanstat
Authors: Morisawa Takeshi , Wong Ronald J. , Bhutani Vinod K. , Vreman Hendrik J. , Stevenson David K. 
Published: October 2008

Inhibition of heme oxygenase (HO), the rate-limiting enzyme in heme catabolism, may be an ideal strategy for preventing neonatal jaundice. Although natural and synthetic heme analogs, called metalloporphyrins (Mps), have been extensively investigated for this purpose, some Mps are phototoxic, affect the activity of other enzymes, or induce HO-1 transcription—properties that may limit their clinical use. Another class of compounds, imidazole–dioxolanes, has been shown to selectively inhibit the inducible isozyme HO-1. Therefore, we investigated the efficacy of azalanstat (AZA), an imidazole–dioxolane, towards inhibiting HO activity in 7-day-old mice. We found that a single dose of AZA at 500 µmol·kg–1body mass (BM) administered i.p. significantly inhibited HO activity and reduced in vivo bilirubin production. In the spleen, HO inhibition (>50%) was observed within 0.25–3 h after administration. After 24 h, however, spleen HO activity, HO-1 protein, and HO-1 mRNA levels significantly increased 1.2-, 2.4-, and 4.0-fold, respectively. We conclude that AZA effectively inhibits in vivo HO activity only at a high dose and that it also induces spleen HO-1 gene transcription. Therefore, other imidazole–dioxolanes should be evaluated to determine whether they are more potent than AZA for use in treating neonatal jaundice.
Effect of crude sulphated polysaccharide from brown algae against acetaminophen-induced toxicity in rats
Authors: Raghavendran Hanumantha Rao Balaji , Srinivasan Periasamy 
Published: October 2008

This study was conducted to examine the protective role of crude polysaccharide from brown seaweed Sargassum polycystum against acetaminophen-induced abnormality in blood glucose, serum albumin/globulin ratio, and liver glycogen, lactate, and pyruvate. Liver and renal tissue histology was performed to confirm the efficacy of Sargassum polysaccharide. A toxic dose of acetaminophen (800 mg/kg body weight intraperitoneally) induced severe abnormality in all basic parameters with apparent toxicity in liver (enlargement of hepatocytes, loss of cytoplasmic content with disruption in the hepatic plates and sinusoidal dilation) and renal tissue (glomerular damage with congestion of tubules). The isolated liver cells were stained with acridine orange and examined under fluorescence microscope, which revealed that the acetaminophen induced significant damage. In contrast, the rats pretreated with Sargassum polysaccharide (200 mg/kg body weight) daily for 3 weeks did not show liver and renal tissue with these severe aberrations induced by acetaminophen. Histology results were also consistent with analyzed basic biochemical parameters, which confirmed the effectiveness of the crude polysaccharide against acetaminophen-induced abnormality in rats.
Chemical sympathetic denervation, suppression of myocardial transient outward potassium current, and ventricular fibrillation in the rat
Authors: Bai Juan , Ren Chongyu , Hao Wei , Wang Rui , Cao Ji-Min 
Published: October 2008

Sympathetic denervation is frequently observed in heart disease. To investigate the linkage of sympathetic denervation and cardiac arrhythmia, we developed a rat model of chemical sympathectomy by subcutaneous injections of 6-hydroxydopamine (6-OHDA). Cardiac sympathetic innervation was visualized by means of a glyoxylic catecholaminergic histofluorescence method. Transient outward current (Ito) of ventricular myocytes was recorded with the whole-cell configuration of the patch clamp technique. We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of Ito channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing. Three weeks after 6-OHDA injections, which allowed time for sympathetic regeneration, we found cardiac sympathetic nerve density, norepinephrine levels, expression levels of Kv4.2 and KChIP2 proteins, and Ito densities were partially normalized and ventricular fibrillation severity was decreased. We conclude that chemical sympathectomy downregulates the expression of selective Kv channel subunits and decreases myocardial Ito channel activities, contributing to the elevated susceptibility to ventricular fibrillation.
Potassium fluxes, energy metabolism, and oxygenation in intact diabetic rat hearts under normal and stress conditions
Authors: Jilkina Olga , Kuzio Bozena , Kupriyanov Valery V. 
Published: October 2008

We evaluated the function of Na+/K+ATPase and sarcolemmal KATPchannels in diabetic rat hearts. Six weeks after streptozotocin (STZ) injection, unidirectional K+fluxes were assayed by using87rubidium (87Rb+) MRS. The hearts were loaded with Rb+by perfusion with Krebs–Henseleit buffer, in which 50% of K+was substituted with Rb+. The rate constant of Rb+uptake via Na+/K+ATPase was reduced. KATP-mediated Rb+efflux was activated metabolically with 2,4-dinitrophenol (DNP, 50 µmol·L–1) or pharmacologically with a KATPchannel opener, P-1075 (5 µmol·L–1). Cardiac energetics were monitored by using31P MRS and optical spectroscopy. DNP produced a smaller ATP decrease, yet similar Rb+efflux activation in STZ hearts. In K+-arrested hearts, P-1075 had no effect on high-energy phosphates and stimulated Rb+efflux by interaction with SUR2A subunit of KATPchannel; this stimulation was greater in STZ hearts. In normokalemic hearts, P-1075 caused cardiac arrest and ATP decline, and the stimulation of Rb+efflux was lower in normokalemic STZ hearts arrested by P-1075. Thus, the Rb+efflux stimulation in STZ hearts was altered depending on the mode of KATPchannel activation: pharmacologic stimulation (P-1075) was enhanced, whereas metabolic stimulation (DNP) was reduced. Both the basal concentration of phosphocreatine ([PCr]) and [PCr]/[ATP] were reduced; nevertheless, the STZ hearts were more or equally resistant to metabolic stress.
Pulmonary feedback and gestational age-dependent regulation of fetal breathing movements
Authors: Hasan Shabih U. , Bharadwaj Baikunth , Remmers John E. , Patel Avni , Rigaux Anita , Schneider Jennifer 
Published: October 2008

Prenatal lung development requires fetal breathing movements (FBM). To investigate the dependence of FBM on feedback originating from the lung, we hypothesized that pneumonectomy stimulates FBM. Time-dated fetal sheep underwent bilateral pneumonectomy, unilateral pneumonectomy, or sham surgery at 125–130 days gestation. The incidence of FBM decreased in sham-operated fetuses at 142 days versus 130 days (p = 0.013), but was unchanged across all gestational ages in bilaterally pneumonectomized fetuses (p ≥ 0.52). In unilaterally pneumonectomized fetuses, the incidence of FBM remained unchanged until 139 days and was higher than that of the bilaterally pneumonectomized fetuses at 130–136 days gestation (p ≤ 0.03). The amplitude of integrated diaphragmatic electromyographic activity (∫EMGdi) and total respiratory output (frequency of breathing × ∫EMGdi) were lower in pneumonectomized fetuses versus sham-operated fetuses at later gestational ages (p < 0.05). These decreases in ∫EMGdiand total respiratory output were most pronounced at 142 days in bilaterally pneumonectomized fetuses versus sham-operated fetuses (p = 0.006 and 0.016, respectively). Low-voltage electrocortical activity (ECoG) increased, and high-voltage ECoG decreased, in unilaterally pneumonectomized fetuses compared with sham-operated fetuses (p = 0.04). In conclusion, we provide new evidence that feedback from the fetal lung modulates the incidence and various components of phrenic nerve output, suggesting a positive feedback mechanism between FBM and lung development.
Fault reactivation in the Port Campbell Embayment with respect to carbon dioxide sequestration, Otway Basin, Australia
Authors: Rogers Claire , van Ruth Peter J. , Hillis Richard R. 
Published: October 2008

Abstract

The Naylor structure in the Port Campbell Embayment, Otway Basin, South Australia is proposed as a demonstration site for the subsurface geological storage of carbon dioxide (CO
2
). The Naylor structure is a fault‐bounded high with normal faults to the north and west to SW. Seismic interpretation shows evidence of recent fault reactivation in the Otway Basin. It is postulated that residual hydrocarbon columns (accumulated and leaked prior to present day) in the Otway Basin leaked due to fault reactivation. Thus, a critical issue in the geological storage of CO
2
in the Port Campbell Embayment is the potential for the reactivation of faults bounding the Naylor structure.

The propensity of faults to be reactivated is assessed by determining the
in‐situ
stress field, the mechanical properties of the fault rock and the orientations of the existing faults. The
in‐situ
stress field lies on the boundary of a strike‐slip and reverse faulting regime in the Port Campbell Embayment. The vertical, minimum horizontal and maximum horizontal stress gradients are 21 MPa km
−1
, 19 MPa km
−1
and 38 MPa km
−1
respectively and the pore pressure gradient is hydrostatic. The maximum horizontal stress in the Port Campbell Embayment is oriented at 150°N.

One planar and two curviplanar faults were identified within the Naylor structure. Two fault segments act to trap accumulations at the crest of the structure. These fault segments have relatively low propensities to reactivate near the crest of the structure. The intended migration pathway of the CO
2
plume does not intersect the identified faults until it reaches the crest of the Naylor structure. However, reservoir heterogeneities such as sub‐seismic faults may cause the migrating CO
2
plume to move towards identified fault segments which are not intended to trap the injected CO
2
and have a relatively high propensity to reactivate.