bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isotopic ecology ten years after a call for more laboratory experiments
Authors: Martínez del Rio Carlos , Wolf Nathan , Carleton Scott A. , Gannes Leonard Z. 
Published: November 2008

AbstractAbout 10 years ago, reviews of the use of stable isotopes in animal ecology predicted explosive growth in this field and called for laboratory experiments to provide a mechanistic foundation to this growth. They identified four major areas of inquiry: (1) the dynamics of isotopic incorporation, (2) mixing models, (3) the problem of routing, and (4) trophic discrimination factors. Because these areas remain central to isotopic ecology, we use them as organising foci to review the experimental results that isotopic ecologists have collected in the intervening 10 years since the call for laboratory experiments. We also review the models that have been built to explain and organise experimental results in these areas.
Src‐protein tyrosine kinases are required for cocaine‐induced increase in the expression and function of the NMDA receptor in the ventral tegmental area
Authors: Schumann Johanna , Michaeli Avner , Yaka Rami 
Published: November 2008

AbstractCocaine‐induced long‐term potentiation of glutamatergic synapses in the ventral tegmental area (VTA) has been proposed as a key process that contributes to the development of addictive behaviors. In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for the initiation of cocaine sensitization. Here we show that application of cocaine both in slices andin vivoinduced an increase in tyrosine phosphorylation of the NR2A, but not the NR2B subunit of the NMDAR in juvenile rats. Cocaine induced an increase in the activity of both Fyn and Src kinases, and the Src‐protein tyrosine kinase (Src‐PTKs) inhibitor, 4‐amino‐5‐(4‐chlorophenyl)‐7‐(t‐butyl)pyrazolo[3,4‐d]pyrimidine (PP2), abolished both cocaine‐induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA. Moreover, cocaine‐induced enhancement in NMDAR‐mediated excitatory post‐synaptic currents was completely abolished by PP2. Taken together, these results suggest that acute cocaine induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A‐containing NMDAR through members of the Src‐PTKs. This in turn, increased NMDAR‐mediated currents in VTA dopamine neurons. These results provide a potential cellular mechanism by which cocaine triggers NMDAR‐dependent synaptic plasticity of VTA neurons that may underlie the development of behavioral sensitization.
Prospective comparison of course of disability in antipsychotic‐treated and untreated schizophrenia patients
Authors: Thirthalli J. , Venkatesh B. K. , Kishorekumar K. V. , Arunachala U. , Venkatasubramanian G. , Subbakrishna D. K. , Gangadhar B. N. 
Published: November 2008

Objective:  To compare the course of disability in schizophrenia patients receiving antipsychotics and those remaining untreated in a rural community.Method:  Of 215 schizophrenia patients identified in a rural south Indian community, 58% were not receiving antipsychotics. Trained raters assessed the disability in 190 of these at baseline and after 1 year. The course of disability in those who remained untreated was compared with that in those who received antipsychotics.Results:  Mean disability scores remained virtually unchanged in those who remained untreated, but showed a significant decline (indicating decrement in disability) in those who continued to receive antipsychotics and in those in whom antipsychotic treatment was initiated (P < 0.001; group × occasion effect). The proportion of patients classified as ‘disabled’ declined significantly in the treated group (P < 0.01), but remained the same in the untreated group.Conclusion:  Disability in untreated schizophrenia patients remains unchanged over time. Treatment with antipsychotics in the community results in a considerable reduction in disability.
Does habitat fragmentation reduce genetic diversity and subpopulation connectivity?
Authors: Mhemmed Gandour , Kamel Hessini , Chedly Abdelly 
Published: November 2008

The estimation of levels of genetic variation has received considerable attention because it is generally thought to be indicative of overall species vitality and the potential for evolutionary responses to environmental changes. Here, we use allozymes markers and two distinct collections ofCakile maritima, an annual species from sandy coastal habitats (2000 generation and 2005 generation collected from 9 populations in their natural habitats), to assess the magnitude of expected genetic change. We compared genetic diversity between generations (all populations combined), and then between populations at each generation.Based on 13 loci scored from the eight enzymes examined, a high genetic diversity was detected at both the population and generation level as compared to other herbaceous species. However, allelic richness reduction in the 2005 generation suggested restricted gene flow and a high risk of future genetic bottlenecks, if larger tracts of coastal areas disappear. Most loci showed deviation from Hardy‐Weinberg equilibrium due to excess of heterozygotes in all populations suggesting that this species has an allogamic mode of reproduction.It appears most likely that this species has experienced a recent decrease in population size, and that genetic drift in small populations has resulted in a loss of alleles occurring at low frequency. Despite the deterioration process, maintenance of high genetic diversity suggests that there are some ecological factors determining population structure.
Revisiting Hydrologic Sampling Strategies for an Accurate Assessment of Hydrologic Connectivity in Humid Temperate Systems
Authors: Ali Geneviève A. , Roy André G. 
Published: November 2008

AbstractHydrologic connectivity is crucial to our understanding of catchment dynamics, yet there is no consensus among hydrologists about what it is exactly, nor is there any unambiguous way of assessing it from field observations. This review is articulated around the questions: (i) what are the main variables to investigate? and (ii) what is the optimal sampling strategy for hydrologic connectivity prediction in humid temperate systems? Because there are multiple definitions for the concept of connectivity, we first identify the major variables to monitor. Then, the ability of several sampling schemes to meet specific criteria is assessed. None of the schemes fully complies with the criteria even if they are combined in a strategic way, and their individual performance is highly dependent on data resolution. While a two‐stage sampling is recommended, it reflects the difficulty in depicting the complex spatial patterns in hydrologic connectivity.
Delayed neovascularization in inflammation‐induced corneal neovascularization in interleukin‐10‐deficient mice
Authors: Samolov Branka , Kvanta Anders , Van Der Ploeg Ingeborg 
Published: November 2008

Abstract.Purpose:  To investigate the potential modulatory role of interleukin‐10 (IL‐10) in the suture model for corneal neovascularization.Methods:  Neovascularized areas were measured on corneal flat‐mounts in IL‐10−/− and wild‐type C57BL6 mice. The inflammatory cellular response was characterized with immunohistochemistry. Gene expression was measured by real‐time polymerase chain reaction.Results:  IL‐10−/− mice showed a delayed neovascular response compared to wild‐type animals at day 6 after suture, when approximately half of the cornea was neovascularized. No apparent differences in inflammatory responses or in messenger RNA (mRNA) expression for proangiogenic factors were detected in IL‐10−/− versus wild‐type mice.Conclusion:  IL‐10 appears to have a proangiogenic effect in the suture model for corneal neovascularization that cannot be explained by either IL‐10’s anti‐inflammatory effect or apparent cross‐talk with the angiogenic factors vascular endothelial growth factor (VEGF)‐A, metalloproteinase (MMP)‐2 and MMP‐9, angiopoietin (Ang)‐1 and Ang‐2.
The inability of Streptococcus mutans and Lactobacillus acidophilus to form a biofilm in vitro on dentine pretreated with ozone
Authors: Knight GM , McIntyre JM , Craig GG , Mulyani  , Zilm PS 
Published: November 2008

AbstractBackground:  The use of ozone therapy in the treatment of dental caries is equivocal. The aim of this study was to use an in vitro model to determine the effects of prior ozone application to dentine on biofilm formation and to measure any associated reduction in bacteria viability.Methods:  Twenty dentine discs were bonded to the bases of 5 mL polycarbonate screw top vials. Ten dentine discs were infused with ozone for 40 seconds, 10 samples remained untreated as a control. The vials were filled with nutrient medium, sterilized and placed into the outflow from a continuous chemostat culture of Streptococcus mutans and Lactobacillus acidophilus for four weeks. At the conclusion of the experiment bacterial growth was monitored by taking optical density readings of the growth medium in each vial and the outer surface of the dentine specimens were examined by scanning electron microscopy as shown by SEM analysis.Results:  Ozone infusion prevented biofilm formation on all the treated samples while there was substantial biofilm present on the control specimens. While the average optical density of the control specimens was almost twice that of the ozone infused dentine (0.710 for the control with a SD of 0.288 and 0.446 for the ozonated samples with a SD of 0.371), the results were not significant (p > 0.05).Conclusions:  This preliminary study has shown that the infusion of ozone into non‐carious dentine prevented biofilm formation in vitro from S. mutans and L. acidophilus over a four‐week period. The possibility exists that ozone treatment may alter the surface wettability of dentine through reaction with organic constituents.
Ascites is a Negative Prognostic Indicator in Chronic Hepatitis in Dogs
Authors: Raffan E. , McCallum A. , Scase T.J. , Watson P.J. 
Published: November 2008

Background:Chronic hepatitis (CH) in dogs is common but little is known about factors associated with survival. Ascites is a well‐recognized negative prognostic indicator in humans.Hypothesis:Ascites is a negative prognostic indicator in CH in dogs.Animals:Thirty‐four dogs with histologically confirmed CH presented to 1 institution between 1996 and 2005.Methods:Retrospective observational study. CH was diagnosed by histopathology of liver tissue according to the WSAVA criteria. Ascites was diagnosed by abdominal ultrasound. The association of ascites with survival from diagnosis or onset of owner‐reported clinical signs until death from any cause or from liver disease was analyzed. Ascitic and nonascitic groups were further analyzed for differences in treatment and sex.Results:Fourteen of 34 dogs had ascites. Survival from diagnosis to death from liver disease was 0.4 months (95% confidence interval [CI], 0.2–0.6) for ascitic dogs and 24.3 months (CI 11.4–37.1) for nonascitic dogs (P< .001), and from onset of signs to death from liver disease was 2.0 months (CI 0.0–5.6) for ascitic dogs and 33.0 months (CI 8.6–57.4) for nonascitic dogs (P= .0020). Diet and spironolactone use differed between groups.Conclusions and Clinical Importance:Ascites is a significant negative prognostic indicator in dogs with CH. Veterinarians and owners can use this information to aid clinical decision making in affected dogs.
Analysis of Human Papillomavirus Type 18 Load and Integration Status from Low-Grade Cervical Lesion to Invasive Cervical Cancer
Authors: Cheung Jo L. K. , Cheung Tak-Hong , Ng Candy W. Y. , Yu Mei Y. , Wong Martin C. S. , Siu Shing-Shun N. , Yim So-Fan , Chan Paul K. S. 
Published: November 2008

ABSTRACT

The clinical value of viral load and integration testing for human papillomavirus (HPV) remains unclear. Data on HPV type 18 (HPV18) is limited. We examined the HPV18 viral load and integration status of 78 women with normal cervix or neoplasia. While the crude viral load appeared to increase with lesion severity, the association was not significant after normalization with sample cellularity. Unlike reports for HPV16, the amino-terminal 1 region of HPV18 E2 was most frequently (71.0%) disrupted, representing the best marker for integration. A substantial proportion (57.1%) of invasive cancers harbored only the episomal genome, thus jeopardizing the clinical value of integration testing. A large proportion (41.7%) of normal/low-grade lesions showed viral integration, suggesting that integration of HPV18 starts early and is unlikely to be a sole determinant for progression. Interpretation of viral load should take into account the form of HPV infection as single infections had significantly higher viral loads than coinfections (
P
= 0.046). More data generated from routinely collected samples are warranted to verify the clinical value of viral load and integration testing. Viral load quantitation for HPV18 is premature for clinical use at this stage.
Classification of Fowl Adenovirus Serotypes by Use of High-Resolution Melting-Curve Analysis of the Hexon Gene Region
Authors: Steer Penelope A. , Kirkpatrick Naomi C. , O'Rourke Denise , Noormohammadi Amir H. 
Published: November 2008

ABSTRACT
Identification of fowl adenovirus (FAdV) serotypes is of importance in epidemiological studies of disease outbreaks and the adoption of vaccination strategies. In this study, real-time PCR and subsequent high-resolution melting (HRM)-curve analysis of three regions of the hexon gene were developed and assessed for their potential in differentiating 12 FAdV reference serotypes. The results were compared to previously described PCR and restriction enzyme analyses of the hexon gene. Both HRM-curve analysis of a 191-bp region of the hexon gene and restriction enzyme analysis failed to distinguish a number of serotypes used in this study. In addition, PCR of the region spanning nucleotides (nt) 144 to 1040 failed to amplify FAdV-5 in sufficient quantities for further analysis. However, HRM-curve analysis of the region spanning nt 301 to 890 proved a sensitive and specific method of differentiating all 12 serotypes. All melt curves were highly reproducible, and replicates of each serotype were correctly genotyped with a mean confidence value of more than 99% using normalized HRM curves. Sequencing analysis revealed that each profile was related to a unique sequence, with some sequences sharing greater than 94% identity. Melting-curve profiles were found to be related mainly to GC composition and distribution throughout the amplicons, regardless of sequence identity. The results presented in this study show that the closed-tube method of PCR and HRM-curve analysis provides an accurate, rapid, and robust genotyping technique for the identification of FAdV serotypes and can be used as a model for developing genotyping techniques for other pathogens.
Identification of Plasmid-Mediated AmpC β-Lactamases in
Escherichia coli
,
Klebsiella
spp., and
Proteus
Species Can Potentially Improve Reporting of Cephalosporin Susceptibility Testing Results
Authors: Tenover Fred C. , Emery Shannon L. , Spiegel Carol A. , Bradford Patricia A. , Eells Samantha , Endimiani Andrea , Bonomo Robert A. , McGowan John E. 
Published: November 2008

ABSTRACT

The goal of this study was to determine if the interpretations of extended-spectrum and advanced-spectrum cephalosporins (ESCs and ASCs, respectively) for isolates of
Enterobacteriaceae
would be impacted by the results of aminophenylboronic acid (APBA) testing. Fifty-three isolates of
Escherichia coli
, 21
Klebsiella
species, and 6
Proteus
species that were resistant to at least one ESC were tested by disk diffusion with ceftazidime and cefotetan disks with and without APBA. Ceftazidime disks with and without clavulanic acid (CLAV) were also tested to confirm extended-spectrum β-lactamase (ESBL) carriage. Twenty-nine (36.3%) isolates were only APBA test positive, 27 were only CLAV test positive, 2 were positive with both substrates, and 22 were negative with both substrates. Thirteen (41.9%) of the 31 APBA-test-positive isolates (all
E. coli
) tested susceptible to cefotaxime, ceftriaxone, or ceftazidime. Since clinical data suggest that AmpC-producing isolates should be reported as resistant to all ESCs, APBA testing can be helpful in identifying such organisms. Screening for AmpC-producing organisms using nonsusceptibility to cefoxitin and amoxicillin-clavulanate was less specific than APBA testing; it identified ESBL as well as AmpC-producing organisms. Only 18 of 31 APBA-positive isolates were positive by PCR for an AmpC β-lactamase gene. Thus, testing with APBA could improve the accuracy of reporting ESCs, especially for
E. coli
. However, results of APBA and CLAV testing did not correlate well for isolates containing both AmpC β-lactamases and ESBLs. Thus, additional data are needed before formal recommendations can be made on changing the reporting of ASC test results.
Expression of vFLIP in a Lentiviral Vaccine Vector Activates NF-κB, Matures Dendritic Cells, and Increases CD8+T-Cell Responses
Authors: Rowe Helen M. , Lopes Luciene , Brown Najmeeyah , Efklidou Sofia , Smallie Timothy , Karrar Sarah , Kaye Paul M. , Collins Mary K. 
Published: November 2008

ABSTRACTLentiviral vectors deliver antigens to dendritic cells (DCs) in vivo, but they do not trigger DC maturation. We therefore expressed a viral protein that constitutively activates NF-κB, vFLIP from Kaposi's sarcoma-associated herpesvirus (KSHV), in a lentivector to mature DCs. vFLIP activated NF-κB in mouse bone marrow-derived DCs in vitro and matured these DCs to a similar extent as lipopolysaccharide; costimulatory markers CD80, CD86, CD40, and ICAM-1 were upregulated and tumor necrosis factor alpha and interleukin-12 secreted. The vFLIP-expressing lentivector also matured DCs in vivo. When we coexpressed vFLIP in a lentivector with ovalbumin (Ova), we found an increased immune response to Ova; up to 10 times more Ova-specific CD8+T cells secreting gamma interferon were detected in the spleens of vFLIP_Ova-immunized mice than in the spleens of mice immunized with GFP_Ova. Furthermore, this increased CD8+T-cell response correlated with improved tumor-free survival in a tumor therapy model. A single immunization with vFLIP_Ova also reduced the parasite load when mice were challenged with OVA-Leishmania donovani. In conclusion, vFLIP from KSHV is a DC activator, maturing DCs in vitro and in vivo. This demonstrates that NF-κB activation is sufficient to induce many aspects of DC maturation and that expression of a constitutive NF-κB activator can improve the efficacy of a vaccine vector.
Distinct Domains within APOBEC3G and APOBEC3F Interact with Separate Regions of Human Immunodeficiency Virus Type 1 Vif
Authors: Russell Rebecca A. , Smith Jessica , Barr Rebekah , Bhattacharyya Darshana , Pathak Vinay K. 
Published: November 2008

ABSTRACT
Human APOBEC3G (A3G) and APOBEC3F (A3F) inhibit the replication of Vif-deficient human immunodeficiency virus type 1 (HIV-1). HIV-1 Vif overcomes these host restriction factors by binding to them and inducing their degradation. Thus, the Vif-A3G and Vif-A3F interactions are attractive targets for antiviral drug development, as inhibiting these interactions could allow the host defense mechanism to control HIV-1 replication. Recently, it has been reported that amino acids 105 to 156 of A3G are involved in the interaction with Vif; however, to date, the region of A3F involved in Vif binding has not been identified. Using our previously reported Vif mutants that are capable of binding to only A3G (3G binder) or only A3F (3F binder), in conjunction with a series of A3G-A3F chimeras, we have now mapped the APOBEC3-Vif interaction domains. We found that the A3G domain that interacts with the Vif YRHHY region is located between amino acids 126 and 132 of A3G, which is consistent with the conclusions reported in previous studies. The A3F domain that interacts with the Vif DRMR region did not occur in the homologous domain but instead was located between amino acids 283 and 300 of A3F. These studies are the first to identify the A3F domain that interacts with the Vif DRMR region and show that distinct domains of A3G and A3F interact with different Vif regions. Pharmacological inhibition of either or both of these Vif-A3 interactions should prevent the degradation of the APOBEC3 proteins and could be used as a therapy against HIV-1.
MAVS Dimer Is a Crucial Signaling Component of Innate Immunity and the Target of Hepatitis C Virus NS3/4A Protease
Authors: Baril Martin , Racine Marie-Eve , Penin François , Lamarre Daniel 
Published: November 2008

ABSTRACT
The mitochondrial antiviral signaling (MAVS) protein plays a central role in innate antiviral immunity. Upon recognition of a virus, intracellular receptors of the RIG-I-like helicase family interact with MAVS to trigger a signaling cascade. In this study, we investigate the requirement of the MAVS structure for enabling its signaling by structure-function analyses and resonance energy transfer approaches in live cells. We now report the essential role of the MAVS oligomer in signal transduction and map the transmembrane domain as the main determinant of dimerization. A combination of mutagenesis and computational methods identified a cluster of residues making favorable van der Waals interactions at the MAVS dimer interface. We also correlated the activation of IRF3 and NF-κB with MAVS oligomerization rather than its mitochondrial localization. Finally, we demonstrated that MAVS oligomerization is disrupted upon expression of HCV NS3/4A protease, suggesting a mechanism for the loss of antiviral signaling. Altogether, our data suggest that the MAVS oligomer is essential in the formation of a multiprotein membrane-associated signaling complex and enables downstream activation of IRF3 and NF-κB in antiviral innate immunity.
Broad-Spectrum Inhibition of Retroviral and Filoviral Particle Release by Tetherin
Authors: Jouvenet Nolwenn , Neil Stuart J. D. , Zhadina Maria , Zang Trinity , Kratovac Zerina , Lee Youngnam , McNatt Matthew , Hatziioannou Theodora , Bieniasz Paul D. 
Published: November 2008

ABSTRACT
The expression of many putative antiviral genes is upregulated when cells encounter type I interferon (IFN), but the actual mechanisms by which many IFN-induced gene products inhibit virus replication are poorly understood. A recently identified IFN-induced antiretroviral protein, termed tetherin (previously known as BST-2 or CD317), blocks the release of nascent human immunodeficiency virus type 1 (HIV-1) particles from infected cells, and an HIV-1 accessory protein, Vpu, acts as a viral antagonist of tetherin. Here, we show that tetherin is capable of blocking not only the release of HIV-1 particles but also the release of particles assembled using the major structural proteins of a variety of prototype retroviruses, including members of the alpharetrovirus, betaretrovirus, deltaretrovirus, lentivirus, and spumaretrovirus families. Moreover, we show that the release of particles assembled using filovirus matrix proteins from Marburg virus and Ebola virus is also sensitive to inhibition by tetherin. These findings indicate that tetherin is a broadly specific inhibitor of enveloped particle release, and therefore, inhibition is unlikely to require specific interactions with viral proteins. Nonetheless, tetherin colocalized with nascent virus-like particles generated by several retroviral and filoviral structural proteins, indicating that it is present at, or recruited to, sites of particle assembly. Overall, tetherin is potentially active against many enveloped viruses and likely to be an important component of the antiviral innate immune defense.