bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ecological Correlates of Extinction Proneness in Australian Tropical Rain Forest Mammals
Authors: LAURANCE WILLIAM F. 
Published: July 2005

Abstract.There is a dire need to predict the vulnerability of tropical forest biotas to habitat fragmentation I tested the efficacy of seven ecological traits (body size Iongeuity, fecundity, trophic level, dietary specialization, natural abundance in rain forest and abundance in the surrounding habitat matrix) for predicting responses of 16 nonflying mammal species to rain forest fragmentation in tropical QueenslaM Australia An ordination analysis revealed that most (84%) of the variation in traits was described by two axes, the first separating rand K‐selected species, and the second discriminating rare species with specialized diets from common species with generalized diets.Using multiple regression analysis, the two ordination axes explained 51.7% of variation in mammal extinction proneness (F = 9.96 P = 0.009). Howem, univariate tests revealed tbat a single trait abundance in the mawas a betterpredictor of vulnerability (r2= 63.8%, F = 24.69, P < 0.001). Partial correlations demonstrated that once the effects of matrix abundance tuete remove4 no other traits or ordination axes were significant predictors of extinction proneness.These results highlight the importance of tolerance of modijied habitats in determining survival of nonpying mammals in tropical forest fragments. Species tbat traverse or exploit modaxied habitats tend to remain stable or inmase in fragments whereas those tbat avoid these habitats often disappem The implications of these findings for hopical forest conservation are discussed.
Effects of Vitamin A Supplementation on Immune Responses and Correlation with Clinical Outcomes
Authors: Villamor Eduardo , Fawzi Wafaie W. 
Published: July 2005

SUMMARYVitamin A supplementation to preschool children is known to decrease the risks of mortality and morbidity from some forms of diarrhea, measles, human immunodeficiency virus (HIV) infection, and malaria. These effects are likely to be the result of the actions of vitamin A on immunity. Some of the immunomodulatory mechanisms of vitamin A have been described in clinical trials and can be correlated with clinical outcomes of supplementation. The effects on morbidity from measles are related to enhanced antibody production and lymphocyte proliferation. Benefits for severe diarrhea could be attributable to the functions of vitamin A in sustaining the integrity of mucosal epithelia in the gut, whereas positive effects among HIV-infected children could also be related to increased T-cell lymphopoiesis. There is no conclusive evidence for a direct effect of vitamin A supplementation on cytokine production or lymphocyte activation. Under certain circumstances, vitamin A supplementation to infants has the potential to improve the antibody response to some vaccines, including tetanus and diphtheria toxoids and measles. There is limited research on the effects of vitamin A supplementation to adults and the elderly on their immune function; currently available data provide no consistent evidence for beneficial effects. Additional studies with these age groups are needed.
Enterotoxigenic
Escherichia coli
in Developing Countries: Epidemiology, Microbiology, Clinical Features, Treatment, and Prevention
Authors: Qadri Firdausi , Svennerholm Ann-Mari , Faruque A. S. G. , Sack R. Bradley 
Published: July 2005

SUMMARY
ETEC is an underrecognized but extremely important cause of diarrhea in the developing world where there is inadequate clean water and poor sanitation. It is the most frequent bacterial cause of diarrhea in children and adults living in these areas and also the most common cause of traveler's diarrhea. ETEC diarrhea is most frequently seen in children, suggesting that a protective immune response occurs with age. The pathogenesis of ETEC-induced diarrhea is similar to that of cholera and includes the production of enterotoxins and colonization factors. The clinical symptoms of ETEC infection can range from mild diarrhea to a severe cholera-like syndrome. The effective treatment of ETEC diarrhea by rehydration is similar to treatment for cholera, but antibiotics are not used routinely for treatment except in traveler's diarrhea. The frequency and characterization of ETEC on a worldwide scale are inadequate because of the difficulty in recognizing the organisms; no simple diagnostic tests are presently available. Protection strategies, as for other enteric infections, include improvements in hygiene and development of effective vaccines. Increases in antimicrobial resistance will dictate the drugs used for the treatment of traveler's diarrhea. Efforts need to be made to improve our understanding of the worldwide importance of ETEC.
Epidemiology and Management of Infectious Diseases in International Adoptees
Authors: Murray Thomas S. , Groth M. Elizabeth , Weitzman Carol , Cappello Michael 
Published: July 2005

SUMMARY
International adoptees represent a group of children with unique health care needs. Data from published studies, along with the recent experience of the Yale International Adoption Clinic, suggest that the risk of serious infections in adoptees is low, although infections associated with institutionalization still occur commonly. Interpretation of these data must be undertaken with caution, however, since many, if not most, international adoptees are not evaluated in specialty clinics. Thus, prospective studies designed to minimize selection and referral bias are needed in order to accurately define the risk of infectious and noninfectious diseases in all international adoptees.
Immune Responses and Disease Enhancement during Respiratory Syncytial Virus Infection
Authors: Openshaw Peter J. M. , Tregoning John S. 
Published: July 2005

SUMMARYRespiratory syncytial virus (RSV) is one of the commonest and most troublesome viruses of infancy. It causes most cases of bronchiolitis, which is associated with wheezing in later childhood. In primary infection, the peak of disease typically coincides with the development of specific T- and B-cell responses, which seem, in large part, to be responsible for disease. Animal models clearly show that a range of immune responses can enhance disease severity, particularly after vaccination with formalin-inactivated RSV. Prior immune sensitization leads to exuberant chemokine production, an excessive cellular influx, and an overabundance of cytokines during RSV challenge. Under different circumstances, specific mediators and T-cell subsets and antibody-antigen immune complex deposition are incriminated as major factors in disease. Animal models of immune enhancement permit a deep understanding of the role of specific immune responses in RSV disease, assist in vaccine design, and indicate which immunomodulatory therapy might be beneficial to children with bronchiolitis.
Novel Perspectives on Mucormycosis: Pathophysiology, Presentation, and Management
Authors: Spellberg Brad , Edwards John , Ibrahim Ashraf 
Published: July 2005

SUMMARYMucormycosis is a life-threatening fungal infection that occurs in immunocompromised patients. These infections are becoming increasingly common, yet survival remains very poor. A greater understanding of the pathogenesis of the disease may lead to future therapies. For example, it is now clear that iron metabolism plays a central role in regulating mucormycosis infections and that deferoxamine predisposes patients to mucormycosis by inappropriately supplying the fungus with iron. These findings raise the possibility that iron chelator therapy may be useful to treat the infection as long as the chelator does not inappropriately supply the fungus with iron. Recent data support the concept that high-dose liposomal amphotericin is the preferred monotherapy for mucormycosis. However, several novel therapeutic strategies are available. These options include combination therapy using lipid-based amphotericin with an echinocandin or with an azole (largely itraconazole or posaconazole) or with all three. The underlying principles of therapy for this disease remain rapid diagnosis, reversal of underlying predisposition, and urgent surgical debridement.
Increased resting heart rate with pollutants in a population based study
Authors: Ruidavets Jean-Bernard , Cassadou Sylvie , Cournot Maxime , Bataille Vincent , Meybeck Mariam , Ferrières Jean 
Published: July 2005

Background:Air pollution is associated with cardiovascular mortality. Changes in the autonomic nervous system may contribute to cardiac arrhythmias and cardiovascular mortality. This study investigated the relations between air pollutant concentrations of sulphur dioxide (SO2), ozone (O3), nitric dioxide (NO2), and resting heart rate (RHR) in a population based study.Methods:A sample of 863 middle aged men and women, living in Toulouse (MONICA centre) area, was randomly recruited. A cross sectional survey on cardiovascular risk factors was carried. RHR was measured twice in a sitting position after a five minute rest. Multivariate analyses with quintiles of RHR were performed using polytomous logistic regression. Models were adjusted for temperature, season, relative humidity, sex, physical activity, blood pressure, C reactive protein, and cardiovascular drugs.Results:For NO2, the OR (odds ratio) (95% CI) associated with an increase of 5 μg/m3in the current day of medical examination was 1.14 (1.03 to 1.25) in quintile Q5 of RHR compared with Q1, p for trend = 0.003. For SO2, OR was 1.16 (0.94 to 1.44) in Q5 compared with Q1, p for trend = 0.05, and for O3, OR was 0.96 (0.91 to 1.01) in Q5 compared with Q1, p for trend = 0.11. No significant association was seen when the daily mean concentration of NO2, SO2, and O3was considered during the previous day as well as when day lag 2 or 3 was considered. The cumulative concentration (three consecutive days) of O3is negatively associated with RHR (p for trend  =  0.02).Conclusion:Changes in pulse rate could reflect cardiac rhythm changes and may be part of the pathophysiological link between pollution and cardiovascular mortality.
MORE ON THE SUM-PRODUCT PHENOMENON IN PRIME FIELDS AND ITS APPLICATIONS
Authors: BOURGAIN J. 
Published: July 2005

In this paper we establish new estimates on sum-product sets and certain exponential sums in finite fields of prime order. Our first result is an extension of the sum-product theorem from [8] when sets of different sizes are involed. It is shown that if [Formula: see text] and pε < |B|, |C| < |A| < p1-ε, then |A + B| + |A · C| > pδ (ε)|A|. Next we exploit the Szemerédi–Trotter theorem in finite fields (also obtained in [8]) to derive several new facts on expanders and extractors. It is shown for instance that the function f(x,y) = x(x+y) from [Formula: see text] to [Formula: see text] satisfies |F(A,B)| > pβ for some β = β (α) > α whenever [Formula: see text] and |A| ~ |B|~ pα, 0 < α < 1. The exponential sum ∑x∈ A,y∈Bεp(axy+bx2y2), ab ≠ 0 ( mod p), may be estimated nontrivially for arbitrary sets [Formula: see text] satisfying |A|, |B| > pρ where ρ < 1/2 is some constant. From this, one obtains an explicit 2-source extractor (with exponential uniform distribution) if both sources have entropy ratio at last ρ. No such examples when ρ < 1/2 seemed known. These questions were largely motivated by recent works on pseudo-randomness such as [2] and [3]. Finally it is shown that if pε < |A| < p1-ε, then always |A + A|+|A-1 + A-1| > pδ(ε)|A|. This is the finite fields version of a problem considered in [11]. If A is an interval, there is a relation to estimates on incomplete Kloosterman sums. In the Appendix, we obtain an apparently new bound on bilinear Kloosterman sums over relatively short intervals (without the restrictions of Karatsuba's result [14]) which is of relevance to problems involving the divisor function (see [1]) and the distribution ( mod p) of certain rational functions on the primes (cf. [12]).
In vivo rabbit acute model tests of polyurethane catheters coated with a novel antithrombin-heparin covalent complex
Authors: Du Ying Jun , Klement Petr , Berry Leslie R. , Tressel Paul , Chan Anthony K. C. 
Published: July 2005

SummaryCatheter use has been associated with an incresed risk of thrombotic complications. The objective was to make catheters less thrombogenic with the use of antithrombin-heparin covalent complex (ATH). The antithrombotic activity of ATH-coated catheters was compared to uncoated (control) and heparincoated catheters in an acute rabbit model of accelerated occluding clot formation. Anaesthetized rabbits were pre-injected with rabbit 125I-fibrinogen,followed by insertion of test catheters into the jugular vein. Blood was drawn and held in a syringe, reinjected, then flushed with saline. The experiment was terminated when blood could no longer be withdrawn (occluding clot). Efficacy was defined as the ability of catheters to remain unoccluded. Clot formation, determined by measuring deposition of radiolabeled fibrin, was a secondary endpoint. ATH-coated catheters were resistant to clotting for the full 240-minute duration, while uncoated and heparin-coated catheters had an average clotting time of 78 and 56 minutes, respectively. The patency ofATH coating was dependant on intact heparin pentasaccharide sequences, rather than the chemistries of the basecoat, the PEO spacer arm, or the antithrombin (AT) protein. The ATH coating was stable to ethylene oxide sterilization, modest abrasion, protease attack, and the coating did not appear to leach off the catheter. Surface tension measurements showed that the ATH modified surface was more hydrophilic than uncoated control catheters or heparin-coated catheters. Thus, ATH-coated catheters are better at preventing clots than uncoated or heparin-coated catheters and show promise as an alternative to the currently available catheters in reducing thrombotic complications associated with its use.
Effect of surface modified liposomes on the aggregation of platelets and tumor cells
Authors: Keil Claudia , Fichtner Iduna , Zeisig Reiner 
Published: July 2005

SummaryMetastasis is still the most serious reason for the high mortality of cancer patients. It is a complex process in which platelets play a crucial role. Several attempts have been performed to inhibit the metastatic process, some of these using modified liposomes. The aggregation behaviour of human platelets and HT29 colon carcinoma cells in the presence of liposomes with a modified surface has been investigated in the present study. Liposomes (PC/CH/DMPE) were unmodified, sterically stabilized by polyethylene glycol (PEG-DSPE), or equipped with the carbohydrate ligand sialyl LewisX (conjugated to PEG-DMPE or DMPE as anchor) intended to specifically compete with ligands expressed by HT29 cells. We found in vitro that an addition of surface modified liposomes to human platelets in plasma caused an up to 2.9-fold increase in platelet aggregation. In addition, when HT29 tumor cells were mixed with platelets and surface modified lipo somes, the number of tumor cells found in aggregates increased significantly from 8.3 % (only tumor cells) to 30.2 %. This result was supported by fluorescence micrographs demonstrating a strong association of platelets and liposomes around the tumor cells. In addition, a clear decrease in number and a change in the distribution of metastases after intravenous injection of HT29 cells in combination with liposomes was observed in vivo. While in control mice metastases in lung, liver and in intestine were prevailing, liposomal treatment resulted in a new localization of metastases in muscles. Taking together, the ability of surface modified liposomes to enhance aggregate formation of platelets and tumor cells has been demonstrated for the first time. The capability of these vesicles to interfere with the metastatic process might have implications for the use of such liposomes for therapeutic applications.
Streptococcus pneumoniae R6x induced p38 MAPK JNK-mediated Caspase-dependent apoptosis in human endothelial cells
Authors: N’Guessan Philippe Dje , Schmeck Bernd , Ayim Abena , Hocke Andreas C. , Brell Bernhard , Hammerschmidt Sven , Rosseau Simone , Suttorp Norbert , Hippenstiel Stefan 
Published: July 2005

Summary
Streptococcus pneumoniae is the major pathogen of communipnetyacquired umonia and a common cause of otitis, meningitis and sepsis. During pneumococci infection accompanied with bacterial invasion and hematogenous spreading, the endothelium is directly targeted by pneumococci and their virulence factors. Therefore, we tested the hypothesis that pneumococci induced endothelial apoptosis. Unencapsulated R6x pneumococci strongly induced apoptosis of human endothelial cells both from lung microvasculature and umbilical vein, whereas an encapsulated strain D39 mainly led to necrotic cell death. Deletion of the gene coding for pneumolysin reduced pneumococci-induced apoptosis in HUVEC. Furthermore, N-acetyl-L-cysteine, an antioxidant thiol, significantly reduced apoptosis caused by R6x, and LDH release induced by D39, pointing to a role for reactive oxygen species in the pathogenesis. Apoptotic cells showed increased cleavage and activity of caspases 6 and 9 but only late activation of caspase 3. Programmed cell death could be strongly reduced by pan-caspase inhibitor zVAD. Reduced levels of Bcl2 and cytosolic increase of apoptosis-inducing factor in pneumococci-infected cells implicated involvement of mitochondrial death pathways. Caspase activation and apoptosis were abolished by cAMP elevation. Moreover, p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase were activated in pneumococci-infected cells and inhibitors of both kinases strongly reduced pneumococci-induced caspase activation and apoptosis. Hence,kinase- and caspase-dependence of pneumococci-induced endothelial apoptosis may bear relevance to novel therapeutic approaches to pneumococci-related disease.
Abciximab therapy is associated with increased platelet activation and decreased heparin dosage in patients with acute myocardial infarction
Authors: Piorkowski Michael , Priess Jana , Weikert Ulf , Jaster Markus , Schwimmbeck Peter-Lothar , Schultheiss Heinz-Peter , Rauch Ursula 
Published: July 2005

SummaryThe inhibition of the glycoprotein (GP) IIb/IIIa receptor for reducing periprocedural ischemic events in patients undergoing coronary intervention is known to influence platelet reactivity. Suboptimal doses of GP IIb/IIIa antagonists have been suggested to be prothrombotic and proinflammatory. This study was performed to observe platelet activation markers, whole blood aggregation and the dosage of unfractionated heparin (UFH) in the presence or absence of the GP IIb/IIIa inhibitor abciximab. Patients with acute myocardial infarction undergoing percutaneous coronary intervention were treated with (n=15) or without (n=15) abciximab. Platelet activation markers were flow cytometrically measured before and after PCI. Whole blood platelet aggregation was tested by a platelet function assay. The patients with abciximab showed a significant increase in platelet activation markers (P-selectin: 7.12 ± 0.36 AU vs 11.05 ± 0.79 AU) and a lower requirement of UFH to prolong aPTT > 60 sec during the infusion. 12 hours after infusion P-selectin level decreased (7.20 ± 0.58 AU), whereas whole blood aggregation was increasing again. After stopping abciximab, requirement of UFH to prolong aPTT increased in the treated group to a greater extent to a level similar to the untreated group even when most of the platelets were still inhibited. The increased platelet activation found at the end of abciximab treatment points to a procoaguable condition that should be carefully monitored and treated by adapting anticoagulation and antiplatelet drugs.
Regulation of platelet guanylyl cyclase by collagen: evidence that Glycoprotein VI mediates platelet nitric oxide synthesis in response to collagen
Authors: Riba Rocio , Sharifi Marzieh , Farndale Richard W. , Khalid M. Naseem 
Published: July 2005

SummaryThe molecular regulation of nitric oxide synthase (NOS) in blood platelets is an uncharacterised area of platelet biology. We investigated the mechanism of collagen-stimulated NO synthesis in platelets. Our aim was to identify the key collagen receptor and downstream signalling mechanisms linking collagen to NOS activation. Collagen and the GpVI-specific platelet activator collagen-related peptide (CRP-XL) stimulated NO synthesis, as evidenced by increased [3H]L-citrulline production, and cyclic GMP (cGMP) formation. After platelet activation by collagen and CRP-XL was normalised, we found no differences in NOS activation or cGMP formation in response to these agonists. Blocking the interaction of collagen with integrin α2β1, a second collagen receptor, failed to affect NOS activation by collagen. These data indicate that collagen-induced NO synthesis is linked to GpVI activation. cGMP formation in response to collagen and CRP-XL required increased intracellular Ca2+, Src family kinases,phosphatidylinositol 3-kinase (PI3-K) and protein kinase C. By comparison, Gp VI-independent cGMP formation induced by thrombin was Src kinase-dependent, but was independent of PI3-K and PKC. Thus the mechanisms of collagen- and CRP-XL-induced NOS activation were identical, but distinct from that of thrombin. Platelet activation in response to collagen leads to secretion of adenosine diphosphate (ADP) and thromboxaneA2 (TxA2). Our results demonstrate that collagenstimulated cGMP synthesis was enhanced significantly by platelet- derived ADP and TxA2. These results reveal that collagen stimulates platelet NOS activation through a specific Ca2+-dependent GpVI receptor signalling cascade,and demonstrate that collagen-induced cGMP accrual requires the release of secondary platelet agonists.
Platelets express steroidogenic 17β–hydroxysteroid dehydrogenases
Authors: Gnatenko Dmitri V. , Cupit Lisa D. , Huang Emily C. , Dhundale Anilkumar , Peter L. Perrotta , Bahou Wadie F. 
Published: July 2005

SummaryHuman blood platelets have important, regulatory functions in diverse hemostatic and pathological disorders, including vascular remodeling, inflammation, and wound repair. Microarray analysis was used to study the molecular basis of essential thrombocythemia, a myeloproliferative disorder with quantitative and qualitative platelet defects associated with cardiovascular and thrombohemorrhagic symptoms, not infrequently neurological. A platelet-expressed gene (HSD17B3) encoding type 3 17β-hydroxysteroid dehydrogenase (previously characterized as a testis-specific enzyme catalyzing the final step in gonadal synthesis of testosterone) was selectively down-regulated in ET platelets, with reciprocal induction of the type 12 enzyme (HSD17B12). Functional 17β-HSD3 activity corresponding to ∼10% of that found in murine testis was demonstrated in normal platelets. The induction of HSD17B12 in ET platelets was unassociated with a concomitant increase in androgen biosynthesis, suggesting distinct functions and/or substrate specificities of the types 3 and 12 enzymes. Application of a molecular assay distinguished ET from normal platelets in 20 consecutive patients (p < 0.0001). These data provide the first evidence that distinct subtypes of steroidogenic 17β−HSDs are functionally present in human blood platelets, and that the expression patterns of HSD17B3 and HSD17B12 are associated with an uncommon platelet disorder manifest by quantitative and qualitative platelet defects.