bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute copper toxicity following copper glycinate injection
Authors: Oon S. , Yap C‐H. , Ihle B. U. 
Published: October 2006

AbstractWe present a patient who developed multi‐organ failure due to severe copper toxicity following attempted suicide by s.c. injection of copper glycinate. Acute copper toxicity is rare in the developed world, although it occurs more frequently in developing world countries, where it is a common mode of suicide. Acute toxicity usually results from oral ingestion and there are several local and systemic effects. Specific management can be difficult as there is little evidence regarding the efficacy of chelating agents in acute toxicity.
Bronchiectasis
Authors: King P. , Holdsworth S. , Freezer N. , Holmes P. 
Published: October 2006

AbstractBronchiectasis is generally classified into cystic fibrosis and non‐cystic fibrosis bronchiectasis. This review article describes non‐cystic fibrosis bronchiectasis in adults. Bronchiectasis can be considered a heterogeneous condition characterized by irreversible airway dilatation with chronic bronchial infection/inflammation. It remains a common condition and is a major cause of respiratory morbidity. Many factors are associated with bronchiectasis, but most commonly patients will have idiopathic disease. Important clinical findings include chronic productive cough, rhinosinusitis, fatigue and bi‐basal crackles. Patients have usually had symptoms for many years. Diagnosis is confirmed by high‐resolution computed tomography scanning using standardized criteria. Spirometry shows moderate airflow obstruction and there is a high prevalence of bronchial hyperreactivity. The most common pathogens are non‐typeable Haemophilus influenzae and Pseudomonas aeruginosa. There may be considerable overlap with other chronic airway diseases. Treatment regimens are still not well defined. Patients tend to have ongoing symptoms and decline in respiratory function despite treatment.
Clinical and quality‐of‐life outcomes in women treated by the TVT‐O procedure
Authors: Lim JL , Cornish A , Carey MP 
Published: October 2006

Objectives To objectively assess the success rate at 6 months after tension‐free vaginal tape obturator (TVT‐O) procedure. To assess subjective success rates, complications, patient satisfaction, and quality of life (QOL).Design A prospective observational study.Setting A tertiary referral urogynaecology practice.Population A cohort of 100 consecutive women who underwent the TVT‐O procedure between March and October 2004.Methods The TVT‐O technique was performed as described. Three standardised QOL questionnaires were completed preoperatively at 6 months and 12 months. At 6 months, a urogenital history, visual analogue scale score (VAS) for patient satisfaction, uroflow, and urinary stress test were performed. After 12 months, a urogenital history and patient satisfaction verbal analogue score (VeAS) were obtained by telephone interview.Main outcome measure Objective success rate of the TVT‐O procedure was measured by negative stress test. Secondary outcomes were subjective success rates at 6 and 12 months, pre‐ and postoperative comparison of urodynamic parameters, complications, postoperative symptomatology, QOL analysis, and patient satisfaction.Results Mean follow up was 18.5 months. Objective success rate was 95%. Subjective success rates were 92 and 84% at 6 and 12 months. Complications included recurrent urinary tract infection (six), voiding difficulty (two), persistent groin discomfort (three), haematoma (one), wound infection (one), vaginal tape erosion (one), and urethral irritation (one). Prevalence of de novo urge incontinence was 4.1 and 4.8% at 6 and 12 months. QOL analysis showed significant improvements in QOL scores postoperatively. Visual and verbal analogue scores indicated high patient satisfaction (VAS, VeAS ≥ 80%) in 77 and 67% at 6 and 12 months.Conclusion The TVT‐O is a safe and effective treatment for female stress urinary incontinence.
Conditioned olfactory responses of a predatory mite, Neoseiulus womersleyi, to volatiles from prey‐infested plants
Authors: Maeda Taro , Liu Yining , Ishiwari Hayato , Shimoda Takeshi 
Published: October 2006

AbstractTo clarify the prey‐finding behavior of the predatory mite Neoseiulus womersleyi (Schicha) (Acari: Phytoseiidae), we studied its olfactory responses to volatiles from the prey‐infested plant on which the mites had been collected. We used a local N. womersleyi population called Kanaya collected from tea (Camellia sinensis L.) (Theaceae) plants infested by Tetranychus kanzawai Kishida (Acari: Tetranychidae) in Kanaya City, Japan. Neoseiulus womersleyi (Kanaya population) were more attracted to volatiles from tea plants infested with five female T. kanzawai per leaf for 7 days than to intact tea leaves in a Y‐tube olfactometer. Tetranychus kanzawai‐induced tea leaf volatiles were identified as (E)‐β‐ocimene, (E)‐4,8‐dimethyl‐1,3,7‐nonatriene, and (E,E)‐α‐farnesene. As olfactory responses are known to differ among local populations of N. womersleyi, we compared the responses of the Kanaya population with those of a Kikugawa population collected from tea plants infested by T. kanzawai in Kikugawa City. To test the influence of previous predation experience, we reared the two populations on tea plants infested by T. kanzawai or on kidney bean plants (Phaseolus vulgaris) infested by Tetranychus urticae Koch. The Kanaya population was more attracted to the volatiles from infested plants on which they had been reared. Because the Kanaya population was not attracted to the plant volatiles they had not previously experienced, the positive response to previously experienced volatiles might be the result of learning. By contrast, the Kikugawa population showed no preference for previously experienced volatiles from infested plants. The implications of this flexibility in foraging behavior are discussed.
Effects of host‐plant species on diapause induction of the Kanzawa spider mite, Tetranychus kanzawai
Authors: Ito Katsura , Saito Yutaka 
Published: October 2006

AbstractIn many herbivorous arthropods, incidence of diapause, which is considered to reflect the timing of diapause, changes depending on the host plants they utilize. Several theoretical studies suggest that the optimal timing of diapause induction depends on life‐history traits; if the development time of the arthropod is short, fecundity is high, or survival rate remains high throughout the season, the optimal timing of diapause induction would be shifted toward the end of the season. For herbivorous arthropods, these life history traits may change among their host plants. Here we examined whether a population of the Kanzawa spider mite, Tetranychus kanzawai Kishida (Acari: Tetranychidae), shows the predicted pattern of diapause induction on two host plants, the kidney bean [Phaseolus vulgaris (Leguminosae)] and Japanese Orixa [Orixa japonica (Rutaceae)], on which the mites show different performances. Rearing conditions were controlled in two ways. In the first experiment, day length and temperature were kept constant throughout the mite lifetime at either of three conditions from mid October to early November. In the second experiment, the conditions were changed from 20 °C and L11.5:D12.5 at immature stages to 18 °C and L11:D13 at adult stage in order to better approximate field conditions. In the first experiment, diapause incidence on P. vulgaris was lower than on O. japonica. This tendency became stronger in the second experiment, suggesting a difference in the timing of diapause induction among host plants. On the other hand, P. vulgaris was proven to allow high performance, i.e., greater lifetime fecundity and shorter development times, although it had no effect on the survival rate. The relationship between diapause incidence and performance is consistent with the prediction of theoretical studies that a short development time or high fecundity delays the timing of diapause induction.
Drosophila melanogaster: the model organism
Authors: Roberts David B. 
Published: October 2006

AbstractIn the 20th century, there were two decades during which Drosophila melanogaster was the most significant model organism and each decade led to the establishment of new scientific disciplines. The first decade was roughly from 1910 and during this period a small group at Columbia University, headed by Thomas Hunt Morgan, established the rules of transmission genetics with which we are all familiar. In the second decade, roughly from 1970, many of the principles and techniques of the earlier period were used to determine the genetic control of basic aspects of the biology of organisms, notably their development and their behaviour. In this review I will show that it was not only the genius of the research workers (five were awarded Nobel Prizes and it has been argued, with justification, that at least one more should have been awarded) but also the special features of D. melanogaster that led to these advances. While Drosophila is still a significant model organism, the advent of molecular biology permits the investigation of organisms less amenable to genetic analysis, but the principles applied in these investigations were in the main principles laid down during the earlier work on Drosophila.
Heterogeneity and Temporal Dynamics of Evolution of G1 Human Rotaviruses in a Settled Population
Authors: Arista Serenella , Giammanco Giovanni M. , De Grazia Simona , Ramirez Stefania , Lo Biundo Concetta , Colomba Claudia , Cascio Antonio , Martella Vito 
Published: October 2006

ABSTRACT
A rotavirus sample collection from 19 consecutive years was used to investigate the heterogeneity and the dynamics of evolution of G1 rotavirus strains in a geographically defined population. Phylogenetic analysis of the VP7 gene sequences of G1P[8] human rotavirus strains showed the circulation of a heterogeneous population comprising three lineages and seven sublineages. Increases in the circulation of G1 rotaviruses were apparently associated with the introduction of novel G1 strains that exhibited multiple amino acid changes in antigenic regions involved in rotavirus neutralization compared to the strains circulating in the previous years. The emergence and/or introduction of G1 antigenic variants might be responsible for the continuous circulation of G1 rotaviruses in the local population, with the various lineages and sublineages appearing, disappearing, or cocirculating in an alternate fashion under the influence of immune-pressure mechanisms. Sequence analysis of VP4-encoding genes of the G1 strains revealed that the older strains were associated with a unique VP4 lineage, while a novel VP4 lineage emerged after 1995. The introduction of human rotavirus vaccines might alter the forces and balances that drive rotavirus evolution and determine the spread of novel strains that are antigenically different from those included in the vaccine formulations. The continuous emergence of VP7-VP4 gene combinations in human rotavirus strains should be taken into consideration when devising vaccination strategies.
PmRab7 Is a VP28-Binding Protein Involved in White Spot Syndrome Virus Infection inShrimp
Authors: Sritunyalucksana Kallaya , Wannapapho Wanphen , Lo Chu Fang , Flegel Timothy W. 
Published: October 2006

ABSTRACT

Our
aim was to isolate and characterize white spot syndrome virus
(WSSV)-binding proteins from shrimp. After a blot of shrimp hemocyte
membrane proteins was overlaid with a recombinant WSSV envelope protein
(rVP28), the reactive bands on the blot were detected using anti-VP28
antibody. Among three membrane-associated molecules identified by
liquid chromatography-tandem mass spectrometry, there was a 25-kDa
protein that bound to both rVP28 and WSSV. Since it had a primary
structure with high homology to the small GTP-binding protein Rab7, we
named it
Penaeus monodon
Rab7 (PmRab7). The full-length PmRab7
cDNA was obtained, and results from a glutathione
S
-transferase pull-down assay confirmed specific binding to
rVP28. Reverse transcriptase PCR analysis revealed PmRab7 expression in
many tissues, and real-time PCR analysis revealed that expression was
constitutive. Binding of PmRab7 to rVP28 or WSSV occurred in a
dose-dependent manner and was inhibited by anti-Rab7 antibody. In an in
vivo neutralization assay, the number of dead shrimp after challenge
with WSSV plus PmRab7 (15%) or WSSV plus anti-Rab7 antibody (5%) was
significantly lower than after challenge with WSSV alone (95%). In
contrast to the WSSV-injected group, shrimp injected with WSSV plus
PmRab7 or WSSV plus anti-Rab7 showed no WSSV-type histopathology. We
conclude that PmRab7 is involved in WSSV infection in shrimp. This is
the first study to identify a shrimp protein that binds directly to a
major viral envelope protein of
WSSV.
Rotavirus Activates JNK and p38 Signaling Pathways in Intestinal Cells, Leading to AP-1-Driven Transcriptional Responses and Enhanced Virus Replication
Authors: Holloway Gavan , Coulson Barbara S. 
Published: October 2006

ABSTRACTRotavirus infection is known to regulate transcriptional changes in many cellular genes. The transcription factors NF-κB and AP-1 are activated by rotavirus infection, but the upstream processes leading to these events are largely unidentified. We therefore studied the activation state during rotavirus infection of c-Jun NH2-terminal kinase (JNK) and p38, which are kinases known to activate AP-1. As assessed by Western blotting using phospho-specific antibodies, infection with rhesus rotavirus (RRV) or exposure to UV-psoralen-inactivated RRV (I-RRV) resulted in the activation of JNK in HT-29, Caco-2, and MA104 cells. Activation of p38 during RRV infection was observed in Caco-2 and MA104 cells but not in HT-29 cells, whereas exposure to I-RRV did not lead to p38 activation in these cell lines. Rotavirus strains SA11, CRW-8, Wa, and UK also activated JNK and p38. Consistent with the activation of JNK, a corresponding increase in the phosphorylation of the AP-1 component c-Jun was shown. The interleukin-8 (IL-8) and c-junpromoters contain AP-1 binding sequences, and these genes have been shown previously to be transcriptionally up-regulated during rotavirus infection. Using specific inhibitors of JNK (SP600125) and p38 (SB203580) and real-time PCR, we showed that maximal RRV-induced IL-8 and c-juntranscription required JNK and p38 activity. This highlights the importance of JNK and p38 in RRV-induced, AP-1-driven gene expression. Significantly, inhibition of p38 or JNK in Caco-2 cells reduced RRV growth but not viral structural antigen expression, demonstrating the potential importance of JNK and p38 activation for optimal rotavirus replication.
Administration of Fludarabine-Loaded Autologous Red Blood Cells in Simian Immunodeficiency Virus-Infected Sooty Mangabeys Depletes pSTAT-1-Expressing Macrophages and Delays the Rebound of Viremia after Suspension of Antiretroviral Therapy
Authors: Cervasi B. , Paiardini M. , Serafini S. , Fraternale A. , Menotta M. , Engram J. , Lawson B. , Staprans S. I. , Piedimonte G. , Perno C. F. , Silvestri G. , Magnani M. 
Published: October 2006

ABSTRACT

A
major limitation of highly active antiretroviral therapy is that it
fails to eradicate human immunodeficiency virus (HIV) infection due to
its limited effects on viral reservoirs carrying replication-competent
HIV, including monocytes/macrophages (M/M). Therefore, therapeutic
approaches aimed at targeting HIV-infected M/M may prove useful in the
clinical management of HIV-infected patients. In previous studies, we
have shown that administration of fludarabine-loaded red blood cells
(RBC) in vitro selectively induces cell death in HIV-infected M/M via a
pSTAT1-dependent pathway. To determine the in vivo efficacy of this
novel therapeutic strategy, we treated six naturally simian
immunodeficiency virus (SIV)-infected sooty mangabeys (SMs) with either
9-[2-(
R
)-(phosphonomethoxy)propyl]adenine (PMPA) only,
fludarabine-loaded RBC only, or PMPA in association with
fludarabine-loaded RBC. The rationale of this treatment was to target
infected M/M with fludarabine-loaded RBC at a time when PMPA is
suppressing viral replication taking place in activated
CD4
+
T cells. In vivo administration of
fludarabine-loaded RBC was well tolerated and did not induce any
discernible side effect. Importantly, addition of fludarabine-loaded
RBC to PMPA delayed the rebound of viral replication after suspension
of therapy, thus suggesting a reduction in the size of SIV reservoirs.
While administrations of fludarabine-loaded RBC did not induce any
change in the CD4
+
or CD8
+
T-cell
compartments, we observed, in chronically SIV-infected SMs, a selective
depletion of M/M expressing pSTAT1. This study suggests that
therapeutic strategies based on the administration of
fludarabine-loaded RBC may be further explored as interventions aimed
at reducing the size of the M/M reservoirs during chronic HIV
infection.
TaxAbolishes Histone H1 Repression of p300 Acetyltransferase Activity at the Human T-Cell Leukemia Virus Type 1Promoter
Authors: Konesky Kasey L. , Nyborg Jennifer K. , Laybourn Paul J. 
Published: October 2006

ABSTRACT

Upon
infection of human T-cell leukemia virus type 1 (HTLV-1), the provirus
is integrated into the host cell genome and subsequently packaged into
chromatin that contains histone H1. Consequently, transcriptional
activation of the virus requires overcoming the environment of
chromatin and H1. To efficiently activate transcription, HTLV-1
requires the virally encoded protein Tax and cellular transcription
factor CREB. Together Tax and CREB interact with three
cis
-acting promoter elements called viral cyclic-AMP response
elements (vCREs). Binding of Tax and CREB to the vCREs promotes
association of p300/CBP into the complex and leads to transcriptional
activation. Therefore, to fully understand the mechanism of Tax
transactivation, it is necessary to examine transcriptional activation
from chromatin assembled with H1. Using a DNA template harboring the
complete HTLV-1 promoter sequence and a highly defined recombinant
assembly system, we demonstrate proper incorporation of histone H1 into
chromatin. Addition of H1 to the chromatin template reduces HTLV-1
transcriptional activation through a novel mechanism. Specifically, H1
does not inhibit CREB or Tax binding to the vCREs or p300 recruitment
to the promoter. Rather, H1 directly targets p300 acetyltransferase
activity. Interestingly, in determining the mechanism of H1 repression,
we have discovered a previously undefined function of Tax, overcoming
the repressive effects of H1-chromatin. Tax specifically abrogates the
H1 repression of p300 enzymatic activity in a manner independent of
p300 recruitment and without displacement of H1 from the
promoter.
Sequential Turnover of Human Immunodeficiency Virus Type 1envthroughout the Course of Infection
Authors: Riddle Tara M. , Shire Norah J. , Sherman Marc S. , Franco Kelly F. , Sheppard Haynes W. , Nelson Julie A. E. 
Published: October 2006

ABSTRACTWe examined the rates of variant population turnover of the V1-V2 and V4-V5 hypervariable domains of the human immunodeficiency virus type 1 (HIV-1) gp120 molecule in longitudinal plasma samples from 14 men with chronic HIV-1 infection using heteroduplex tracking assays (HTA). Six men had high rates of CD4+T-cell loss, and eight men had low rates of CD4+T-cell loss over 2.5 to 8 years of infection. We found that V1-V2 and V4-V5envpopulations changed dramatically over time in all 14 subjects; the changes in these regions were significantly correlated with each another over time. The subjects with rapid CD4 loss had significantly less change in theirenvpopulations than the subjects with slow CD4 loss. The two subjects with rapid CD4 loss and sustained low CD4 counts (<150/μl for at least 2 years) showed stabilization of their V1-V2 and V4-V5 populations as reflected by low levels of total change in HTA pattern and low HTA indices (a novel measure of the emergence of new bands and band distribution); this stabilization was not observed in other subjects. The stabilization ofenvvariant populations at low CD4 counts following periods of rapid viral evolution suggests that selective pressure onenv, likely from new immune responses, is minimal when CD4 counts drop dramatically and remain low for extended periods of time.
Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells Activates Hypoxia-Induced Factors
Authors: Carroll Patrick A. , Kenerson Heidi L. , Yeung Raymond S. , Lagunoff Michael 
Published: October 2006

ABSTRACT
Kaposi's sarcoma-associated herpesvirus (KSHV or HHV-8) is the etiological agent of Kaposi's sarcoma, a highly vascularized, endothelial-derived tumor. A direct role for KSHV-mediated induction of angiogenesis has been proposed based upon the nature of the neoplasia and various KSHV gene overexpression and infection model systems. We have found that KSHV infection of endothelial cells induces mRNA of hypoxia-induced factor 1α (HIF1α) and HIF2α, two homologous alpha subunits of the heterodimeric transcription factor HIF. HIF is a master regulator of both developmental and pathological angiogenesis, composed of an oxygen-sensitive alpha subunit and a constitutively expressed beta subunit. HIF is classically activated posttranscriptionally with hypoxia, leading to increased protein stability of HIF1α and/or HIF2α. However, we demonstrate that both alpha subunits are up-regulated at the transcript level by KSHV infection. The transcriptional activation of HIF leads to a functional increase in HIF activity under normoxic conditions, as demonstrated by both luciferase reporter assay and the increased expression of vascular endothelial growth factor receptor 1 (VEGFR1), an HIF-responsive gene. KSHV infection synergizes with hypoxia mimics and induces higher expression levels of HIF1α and HIF2α protein, and HIF1α is increased in a significant proportion of the latently infected endothelial cells. Src family kinases are required for the activation of HIF and the downstream gene VEGFR1 by KSHV. We also show that KS lesions, in vivo, express elevated levels of HIF1α and HIF2α proteins. Thus, KSHV stimulates the HIF pathway via transcriptional up-regulation of both HIF alphas, and this activation may play a role in KS formation, localization, and progression.
Identification of a Novel Nonstructural Protein, VP9, from White Spot Syndrome Virus: Its Structure Reveals a Ferredoxin Fold with Specific Metal Binding Sites
Authors: Liu Yang , Wu Jinlu , Song Jianxing , Sivaraman J. , Hew Choy L. 
Published: October 2006

ABSTRACT

White spot syndrome virus (WSSV) is a major pathogen in shrimp aquaculture. VP9, a full-length protein of WSSV, encoded by open reading frame wsv230, was identified for the first time in the infected
Penaeus monodon
shrimp tissues, gill, and stomach as a novel, nonstructural protein by Western blotting, mass spectrometry, and immunoelectron microscopy. Real-time reverse transcription-PCR demonstrated that the transcription of VP9 started from the early to the late stage of WSSV infection as a major mRNA species. The structure of full-length VP9 was determined by both X-ray and nuclear magnetic resonance (NMR) techniques. It is the first structure to be reported for WSSV proteins. The crystal structure of VP9 revealed a ferredoxin fold with divalent metal ion binding sites. Cadmium sulfate was found to be essential for crystallization. The Cd
2+
ions were bound between the monomer interfaces of the homodimer. Various divalent metal ions have been titrated against VP9, and their interactions were analyzed using NMR spectroscopy. The titration data indicated that VP9 binds with both Zn
2+
and Cd
2+
. VP9 adopts a similar fold as the DNA binding domain of the papillomavirus E2 protein. Based on our present investigations, we hypothesize that VP9 might be involved in the transcriptional regulation of WSSV, a function similar to that of the E2 protein during papillomavirus infection of the host cells.