bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Surface Enolase Participates in Borrelia burgdorferi-Plasminogen Interaction and Contributes to Pathogen Survival within Feeding Ticks
Authors: Nogueira Sarah Veloso , Smith Alexis A. , Qin Jin-Hong , Pal Utpal 
Published: October 2011

ABSTRACT

Borrelia burgdorferi
, a tick-borne bacterial pathogen, causes a disseminated infection involving multiple organs known as Lyme disease. Surface proteins can directly participate in microbial virulence by facilitating pathogen dissemination via interaction with host factors. We show here that a fraction of the
B. burgdorferi
chromosomal gene product BB0337, annotated as enolase or phosphopyruvate dehydratase, is associated with spirochete outer membrane and is surface exposed.
B. burgdorferi
enolase, either in a recombinant form or as a membrane-bound native antigen, displays enzymatic activities intrinsic to the glycolytic pathway. However, the protein also interacts with host plasminogen, potentially leading to its activation and resulting in
B. burgdorferi
-induced fibrinolysis. As expected, enolase displayed consistent expression
in vivo
, however, with a variable temporal and spatial expression during spirochete infection in mice and ticks. Despite an extracellular exposure of the antigen and a potential role in host-pathogen interaction, active immunization of mice with recombinant enolase failed to evoke protective immunity against subsequent
B. burgdorferi
infection. In contrast, enolase immunization of murine hosts significantly reduced the acquisition of spirochetes by feeding ticks, suggesting that the protein could have a stage-specific role in
B. burgdorferi
survival in the feeding vector. Strategies to interfere with the function of surface enolase could contribute to the development of novel preventive measures to interrupt the spirochete infection cycle and reduce the incidences of Lyme disease.
Interleukin-23-Mediated Inflammation in Pseudomonas aeruginosa Pulmonary Infection
Authors: Dubin Patricia J. , Martz Ashley , Eisenstatt Jessica R. , Fox Michael D. , Logar Alison , Kolls Jay K. 
Published: October 2011

ABSTRACTPseudomonas aeruginosais an opportunistic pathogen that is capable of causing acute and chronic pulmonary infection in the immunocompromised host. In the case of cystic fibrosis (CF), chronicP. aeruginosainfection causes increased mortality by promoting overly exuberant airway inflammation and cumulative lung damage. Identifying the key regulators of this inflammation may lead to the development of new therapies that improveP. aeruginosa-related mortality. We report here that interleukin-23 (IL-23), the cytokine most clearly tied to IL-17-mediated inflammation, also promotes IL-17-independent inflammation duringP. aeruginosapulmonary infection. During the early innate immune response, prior to IL-17 induction, IL-23 acts synergistically with IL-1β to promote early neutrophil (polymorphonuclear leukocyte [PMN]) recruitment. However, at later time points, IL-23 also promoted IL-17 production by lung γδ T cells, which was greatly augmented in the presence of IL-1β. These studies show that IL-23 controls two independent phases of neutrophil recruitment in response toP. aeruginosainfection: early PMN emigration that is IL-17 independent and later PMN emigration regulated by IL-17.
The ‘Twinkie Defense’: the relationship between carbonated non-diet soft drinks and violence perpetration among Boston high school students
Authors: Solnick Sara J , Hemenway David 
Published: October 2011

ObjectivesTo investigate the association of carbonated non-diet soft drink consumption and violence perpetration in a sample of Boston adolescents.MethodsIn a survey of Boston public high schools, respondents were asked how often they drank non-diet soft drinks and whether they had carried a weapon or engaged in physical violence with a peer. Regression analysis was used to determine the role of soft drink consumption in these behaviours.ResultsAdolescents who drank more than five cans of soft drinks per week (nearly 30% of the sample) were significantly more likely to have carried a weapon and to have been violent with peers, family members and dates (p<0.01 for carrying a weapon and p<0.001 for the three violence measures). Frequent soft drink consumption was associated with a 9–15% point increase in the probability of engaging in aggressive actions, even after controlling for gender, age, race, body mass index, typical sleep patterns, tobacco use, alcohol use and having family dinners.ConclusionsThere was a significant and strong association between soft drinks and violence. There may be a direct cause-and-effect relationship, perhaps due to the sugar or caffeine content of soft drinks, or there may be other factors, unaccounted for in our analyses, that cause both high soft drink consumption and aggression.
Post-rift compression on the SW Iberian margin (eastern North Atlantic): a case for prolonged inversion in the ocean–continent transition zone
Authors: Pereira Ricardo , Alves Tiago M. , Cartwright Joe 
Published: October 2011

Abstract:
An extensive grid of 2D seismic reflection data imaging the non-volcanic continental margin of SW Iberia is used to investigate the post-rift compressional evolution in the transition zone between continental and oceanic crust. Tectonic compression affected the margin almost continuously since the latest Cretaceous, but was predominantly focused during the mid-Eocene and the late Oligocene–mid-Miocene. The detailed interpretation of post-rift structures and their adjacent strata shows that crustal shortening in the various sectors of the margin is neither synchronous nor similar in style. Main post-rift structures include: (1) thick-skinned transpressional deformation on the distal margin; (2) localized basin shortening on the outer proximal margin; (3) limited reverse faulting and inversion on the inner proximal margin. The location and magnitude of crustal shortening are dependent on the inherited syn-rift geometry, the existence of evaporite (or clay-rich) detachments at depth, the rheological behaviour of previously extended continental crust and the position of the ocean–continent transition zone. The mechanisms of compression are mainly dominated by plate collision associated with the southeastern migration of the Iberian microplate during the Alpine orogeny and with recent westward convergence with the oceanic domain.
Contrasting styles of mineralization in the Chinese Altai and East Junggar, NW China: implications for the accretionary history of the southern Altaids
Authors: Wan Bo , Xiao Wenjiao , Zhang Lianchang , Windley Brian F. , Han Chunming , Quinn Cameron D. 
Published: October 2011

Abstract:

The Chinese Altai–East Junggar collage in the southern Altaids hosts three metallogenic belts, which are, from north to south: (1) a volcanogenic massive sulphide (VMS) Cu–Pb–Zn belt; (2) a belt of shear zone-related gold deposits; (3) a porphyry Cu–Au–Mo belt. The VMS deposits formed in two pulses (
c
. 405 Ma and
c
. 375 Ma) in the Chinese Altai arc. The porphyry deposits developed in three pulses in the East Junggar arc, the first two synchronous with the VMS mineralization, and the third at
c
. 330 Ma. The shear zone-related gold deposits developed in the late Carboniferous to Permian at the contact between the Chinese Altai and East Junggar arcs. Time–space distributions of diverse ore deposits across the Altai–East Junggar collage indicate that the collage developed from two independent arcs, the Chinese Altai and the East Junggar. The VMS and porphyry deposits developed in the Chinese Altai and East Junggar arcs, respectively. The Chinese Altai arc is interpreted to be a Japanese-type arc, and the East Junggar arc a Mariana-type arc. During the latest Palaeozoic, the two arcs were juxtaposed by the Erqis Fault, when many shear zone-related lode gold deposits were emplaced. These metallogenic distributions were a likely response to spatially localized mechanisms of crust growth and to the tectonic evolution of the Altai–East Junggar collage, and they are consistent with interpretation of the Altaids as a multiple subduction–accretion collage.
Pleistocene giant slope failures offshore Arauco Peninsula, Southern Chile
Authors: Geersen Jacob , Völker David , Behrmann Jan H. , Reichert Christian , Krastel Sebastian 
Published: October 2011

Abstract:

Three Pleistocene giant slope failures are observed in high-resolution bathymetric and seismic reflection data off Southern Chile, two of which extend across the full width of the continental slope from the shelf break to the trench. With mobilized volumes between 253 km
3
and 472 km
3
, these slides are among the largest submarine landslides documented at active continental margins so far. Deposits of each of the slides are imaged as chaotic sequences in seismic reflection lines buried beneath well-stratified sediments in the Chile Trench. The ages of the three slides are about 0.25, 0.41 and >0.56 Ma. The main preconditioning factor for the slope instabilities seems to be local uplift of the continental slope that results in peculiarly high slope angles of up to 30°. Uplift of the marine and continental forearc of the study area is the result of shortening across upper plate faults and therefore a long-term continuous process. Slope instability seems to be an iterative process and failure is likely to recur.
Chemotherapeutic Properties of Phospho-Nonsteroidal Anti-Inflammatory Drugs, a New Class of Anticancer Compounds
Authors: Huang Liqun , Mackenzie Gerardo G. , Sun Yu , Ouyang Nengtai , Xie Gang , Vrankova Kvetoslava , Komninou Despina , Rigas Basil 
Published: October 2011

AbstractNonsteroidal anti-inflammatory drugs (NSAID) exhibit antineoplastic properties, but conventional NSAIDs do not fully meet safety and efficacy criteria for use as anticancer agents. In this study, we evaluated the chemotherapeutic efficacy of 5 novel phospho-NSAIDs, each of which includes in addition to the NSAID moiety a diethylphosphate linked through a butane moiety. All 5 compounds inhibited the growth of human breast, colon, and pancreatic cancer cell lines with micromolar potency. In vivo investigations confirmed the antitumor activity of phospho-aspirin (PA) and phospho-sulindac (PS) in inhibiting tumor growth in established human xenograft models, in which cell proliferation was suppressed and apoptosis enhanced in the absence of detectable animal toxicity. Notably, all of the phospho-NSAIDs tested induced reactive oxygen and nitrogen species in cultured cells, with PA and PS inducing detectable levels of oxidative stress in vivo that were associated positively with apoptosis and negatively with proliferation. Potentially explaining these effects, all of the phospho-NSAIDs tested also inhibited the thioredoxin system and the redox sensitive transcription factor NF-κB. Taken together, our findings show the strong anticancer efficacy and promising safety of phospho-NSAIDs in preclinical models of breast, colon, and pancreatic cancer, suggesting further evaluation as anticancer agents. Cancer Res; 71(24); 7617–27. ©2011 AACR.
Outcomes After In-Hospital Cardiac Arrest in Children With Cardiac Disease
Authors: Ortmann Laura , Prodhan Parthak , Gossett Jeffrey , Schexnayder Stephen , Berg Robert , Nadkarni Vinay , Bhutta Adnan ,   The American Heart Association GWTG-R Investigators, Mancini Mary E. , Berg Robert A. , Allen Emilie , Hunt Elizabeth A. , Nadkarni Vinay M. , Ornato Joseph P. , Braithwaite R. Scott , Nichol Graham , Duncan Kathy , Truitt Tanya L. , Eigel Brian , Laussen Peter C. , Moler Frank W. , Morris Marilyn , Parshuram Chris 
Published: October 2011

Background—
Small studies suggest that children experiencing a cardiac arrest after undergoing cardiac surgery have better outcomes than other groups of patients, but the survival outcomes and periarrest variables of cardiac and noncardiac pediatric patients have not been compared.

Methods and Results—
All cardiac arrests in patients <18 years of age were identified from Get With the Guidelines–Resuscitation from 2000 to 2008. Cardiac arrests occurring in the neonatal intensive care unit were excluded. Of 3323 index cardiac arrests, 19% occurred in surgical-cardiac, 17% in medical-cardiac, and 64% in noncardiac (trauma, surgical-noncardiac, and medical-noncardiac) patients. Survival to hospital discharge was significantly higher in the surgical-cardiac group (37%) compared with the medical-cardiac group (28%; adjusted odds ratio, 1.8; 95% confidence interval, 1.3–2.5) and the noncardiac group (23%; adjusted odds ratio, 1.8; 95% confidence interval, 1.4–2.4). Those in the cardiac groups were younger and less likely to have preexisting noncardiac organ dysfunction, but were more likely to have ventricular arrhythmias as their first pulseless rhythm, to be monitored and hospitalized in the intensive care unit at the time of cardiac arrest, and to have extracorporeal cardiopulmonary resuscitation compared with those in the noncardiac group. There was no survival advantage for patients in the medical-cardiac group compared with those in the noncardiac group when adjusted for periarrest variables.

Conclusion—
Children with surgical-cardiac disease have significantly better survival to hospital discharge after an in-hospital cardiac arrest compared with children with medical-cardiac disease and noncardiac disease.
Long-Term Effects of Percutaneous Coronary Intervention of the Totally Occluded Infarct-Related Artery in the Subacute Phase After Myocardial Infarction
Authors: Hochman Judith S. , Reynolds Harmony R. , Džavík Vladimír , Buller Christopher E. , Ruzyllo Witold , Sadowski Zygmunt P. , Maggioni Aldo P. , Carvalho Antonio C. , Rankin James M. , White Harvey D. , Goldberg Suzanne , Forman Sandra A. , Mark Daniel B. , Lamas Gervasio A. 
Published: October 2011

Background—
Despite observations suggesting a benefit for late opening of totally occluded infarct-related arteries after myocardial infarction, the Occluded Artery Trial (OAT) demonstrated no reduction in the composite of death, reinfarction, and class IV heart failure over a 2.9-year mean follow-up. Follow-up was extended to determine whether late trends would favor either treatment group.

Methods and Results—

OAT randomized 2201 stable patients with infarct-related artery total occlusion >24 hours (calendar days 3–28) after myocardial infarction. Patients with severe inducible ischemia, rest angina, class III-IV heart failure, and 3-vessel/left main disease were excluded. We conducted extended follow-up of enrolled patients for an additional 3 years for the primary end point and angina (6-year median survivor follow-up; longest, 9 years; 12 234 patient-years). Rates of the primary end point (hazard ratio, 1.06; 95% confidence interval, 0.88–1.28), fatal and nonfatal myocardial infarction (hazard ratio, 1.25; 95% confidence interval, 0.89–1.75), death, and class IV heart failure were similar for the percutaneous coronary intervention (PCI) and medical therapy alone groups. No interactions between baseline characteristics and treatment group on outcomes were observed. The vast majority of patients at each follow-up visit did not report angina. There was less angina in the PCI group through early in follow-up; by 3 years, the between group difference was consistently <4 patients per 100 treated and not significantly different, although there was a trend toward less angina in the PCI group at 3 and 5 years. The 7-year rate of PCI of the infarct-related artery during follow-up was 11.1% for the PCI group compared with 14.7% for the medical therapy alone group (hazard ratio, 0.79; 95% confidence interval, 0.61–1.01;
P
=0.06).

Conclusions—
Extended follow-up of the OAT cohort provides robust evidence for no reduction of long-term rates of clinical events after routine PCI in stable patients with a totally occluded infarct-related artery and without severe inducible ischemia in the subacute phase after myocardial infarction.

Clinical Trial Registration—

http://www.clinicaltrials.gov
. Unique identifier: NCT00004562.
The Development of Myocardial Fibrosis in Transgenic Mice With Targeted Overexpression of Tumor Necrosis Factor Requires Mast Cell–Fibroblast Interactions
Authors: Zhang Weili , Chancey Amanda L. , Tzeng Huei-Ping , Zhou Zhenqing , Lavine Kory J. , Gao Feng , Sivasubramanian Natarajan , Barger Philip M. , Mann Douglas L. 
Published: October 2011

Background—
Transgenic mice with cardiac-restricted overexpression of tumor necrosis factor (MHCsTNF mice) develop progressive myocardial fibrosis, diastolic dysfunction, and adverse cardiac remodeling. Insofar as tumor necrosis factor (TNF) does not directly stimulate fibroblast collagen synthesis, we asked whether TNF-induced fibrosis was mediated indirectly through interactions between mast cells and cardiac fibroblasts.

Methods and Results—

Cardiac mast cell number increased 2 to 3 fold (
P
<0.001) in MHCsTNF mice compared with littermate controls. Outcrossing MHCsTNF mice with mast cell–deficient (c-kit
−/−
) mice showed that the 11-fold increase (
P
<0.001) in collagen volume fraction in MHCsTNF/c-kit
+/−
mice was abrogated in MHCsTNF/c-kit
−/−
mice, and that the leftward shifted left ventricular pressure–volume curve in the MHCsTNF/c-kit
+/−
mice was normalized in the MHCsTNF/c-kit
−/−
hearts. Furthermore, the increase in transforming growth factor β1 and type I transforming growth factor β receptor messenger RNA levels was significantly (
P
=0.03,
P
=0.01, respectively) attenuated in MHCsTNF/c-kit
−/−
when compared with MHCsTNF/c-kit
+/−
mice. Coculture of fibroblasts with mast cells resulted in enhanced α-smooth muscle actin expression, increased proliferation and collagen messenger RNA expression, and increased contraction of 3-dimensional collagen gels in MHCsTNF fibroblasts compared with littermate fibroblasts. The effects of mast cells were abrogated by type I transforming growth factor β receptor antagonist NP-40208.

Conclusions—
These results suggest that increased mast cell density with resultant mast cell–cardiac fibroblast cross-talk is required for the development of myocardial fibrosis in inflammatory cardiomyopathy. Cardiac fibroblasts exposed to sustained inflammatory signaling exhibit an increased repertoire of profibrotic phenotypic responses in response to mast cell mediators.
Chelation of aluminum by combining deferasirox and deferiprone in rats
Authors: Saljooghi Amir Shokooh 
Published: October 2011

The hypothesis that two known chelators deferasirox and deferiprone (L1) might be more efficient as combined treatment than as single therapies in removing aluminum from the body was tested in a new acute rat model. Seven-week-old male Wistar rats received chelators: deferasirox (orally [p.o.]), L1 (p.o.) or deferasirox + L1 as 100 or 200 mg/kg dose half an hour after a single intraperitoneal administration of 6 mg Al/kg body weight in the form of chloride. Serum aluminum concentration, urinary aluminum and iron excretions were determined by graphite furnace atomic absorption spectrometry. Both chelators were effective only at the higher dose level. While deferasirox was more effective than L1 in enhancing urinary aluminum excretion, L1 was more effective than deferasirox in enhancing urinary iron excretion. In the combined treatment group, deferasirox did not increase the L1 effect on aluminum and L1 did not increase the effect of deferasirox on iron elimination. Our results support the usefulness of this animal model for preliminary in vivo testing of aluminum chelators. Urinary values were more useful due to the high variability of serum results.
SSRI-induced coagulopathy: is it reality?
Authors: Siddiqui Riyaz , Gawande Sushil , Shende Tanaji , Tadke Rahul , Bhave Sudhir , Kirpekar Vivek 
Published: October 2011

Objectives: To study the effect of escitalopram and fluoxetine on coagulation profile in patients with major depression. Method: This was a prospective, open-label, single-centre study in 40 patients diagnosed with major depressive disorder. The patients were diagnosed using Diagnostic and Statistical Manual of Mental Disorders, fourth edition criteria. Twenty patients receiving escitalopram 10 mg per day and 20 patients receiving fluoxetine 20 mg per day participated in the study and were followed up for 3 months. Coagulation parameters – bleeding time, clotting time, platelet count, prothrombin time and partial thromboplastin kaolin time – were evaluated at baseline and after 3 months. Results: At the end of 3 months, a significant increase in bleeding time was seen in patients receiving fluoxetine, but within the normal range. No rise was seen in the group given escitalopram. Conclusion: In patients with depression, fluoxetine increases bleeding time whereas escitalopram has no effect on coagulation profile. However, both the drugs can be used safely for long-term treatment.
Early and late effects of the DPP-4 inhibitor vildagliptin in a rat model of post-myocardial infarction heart failure
Authors: Yin Meimei , Silljé Herman HW , Meissner Maxi , van Gilst Wiek H , de Boer Rudolf A 
Published: October 2011

Abstract

Background
Progressive remodeling after myocardial infarction (MI) is a leading cause of morbidity and mortality. Recently, glucagon-like peptide (GLP)-1 was shown to have cardioprotective effects, but treatment with GLP-1 is limited by its short half-life. It is rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4), an enzyme which inhibits GLP-1 activity. We hypothesized that the DPP-4 inhibitor vildagliptin will increase levels of GLP-1 and may exert protective effects on cardiac function after MI.

Methods
Sprague-Dawley rats were either subjected to coronary ligation to induce MI and left ventricular (LV) remodeling, or sham operation. Parts of the rats with an MI were pre-treated for 2 days with the DPP-4 inhibitor vildagliptin (MI-Vildagliptin immediate, MI-VI, 15 mg/kg/day). The remainder of the rats was, three weeks after coronary artery ligation, subjected to treatment with DPP-4 inhibitor vildagliptin (MI-Vildagliptin Late, MI-VL) or control (MI). At 12 weeks, echocardiography and invasive hemodynamics were measured and molecular analysis and immunohistochemistry were performed.

Results
Vildagliptin inhibited the DPP-4 enzymatic activity by almost 70% and increased active GLP-1 levels by about 3-fold in plasma in both treated groups (p < 0.05 vs. non-treated groups). Cardiac function (ejection fraction) was decreased in all 3 MI groups compared with Sham group (p < 0.05); treatment with vildagliptin, either early or late, did not reverse cardiac remodeling. ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide) mRNA levels were significantly increased in all 3 MI groups, but no significant reductions were observed in both vildagliptin groups. Vildagliptin also did not change cardiomyocyte size or capillary density after MI. No effects were detected on glucose level and body weight in the post-MI remodeling model.

Conclusion
Vildagliptin increases the active GLP-1 level via inhibition of DPP-4, but it has no substantial protective effects on cardiac function in this well established long-term post-MI cardiac remodeling model.