bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemagglutination Test for Rapid Serodiagnosis of Human Pythiosis
Authors: Jindayok Thanyasiri , Piromsontikorn Savittree , Srimuang Somboon , Khupulsup Kalayanee , Krajaejun Theerapong 
Published: June 2009

ABSTRACTHuman pythiosis is an emerging, life-threatening infectious disease, caused by the oomycetePythium insidiosum. Thailand is an area where human pythiosis is endemic and the genetic blood disorder thalassemia is a predisposing factor. Patients with pythiosis present with arterial occlusions of the lower extremities, corneal ulcers, or chronic cutaneous infections. Diagnosis relies on time-consuming, relatively insensitive tests such as culture identification and immunodiffusion assay. Most patients undergo surgical removal of infected organs, and many die from the infection. Delayed diagnosis results in a poor prognosis. Here, we describe a hemagglutination (HA) test for rapid diagnosis of human pythiosis. Sheep red blood cells were coated withP. insidiosumprotein extract and used in duplicated detection assays using serum samples from 33 patients with vascular (n= 27), cutaneous (n= 2), or ocular (n= 4) pythiosis and serum samples from 289 control patients with other infectious diseases (n= 77), with highly positive antinuclear antibody (n= 5), with thalassemia (n= 21), or with no known disorder (i.e., healthy blood donors) (n= 186). Based on receiver-operating characteristic analysis, a serum titer of 1:160 was selected as the cutoff point for the HA test. Serum samples that generated HA at the cutoff titer were read as positive, while samples that did not were read as negative. Positive results were obtained with the serum samples of all patients with vascular and cutaneous pythiosis and with two serum samples from the control group. Negative results were obtained with serum samples from all ocular pythiosis patients and the 287 remaining serum samples from the control group. Sensitivity and specificity of the HA were 88% and 99%, respectively. In conclusion, the HA test for detection of anti-Pythiumantibodies is a simple, rapid, and reliable test for serodiagnosis of vascular and cutaneous pythiosis.
Recovery of Anti-
Toxoplasma gondii
Immunoglobulin M in Stored Guthrie Card Blood Spots
Authors: Tan Hooi-Kuan , Petersen Eskild , Møller Lone N. , Phillips Pamela , Neto Eurico Camargo , Gilbert Ruth E. 
Published: June 2009

ABSTRACT

Retrospective testing of neonatal Guthrie card blood spots for specific immunoglobulin M (IgM) can distinguish congenital toxoplasmosis from acquired toxoplasmosis. We determined whether storage temperature reduced IgM detection, using filter paper blood samples “spiked” with anti-
Toxoplasma
IgM. After 300 days, IgM detection deteriorated with storage at room temperature but not at temperatures of 4°C or lower.
Polyomavirus Shedding in the Stool of Healthy Adults
Authors: Vanchiere John A. , Abudayyeh Suhaib , Copeland Christina M. , Lu Lee B. , Graham David Y. , Butel Janet S. 
Published: June 2009

ABSTRACT

We recently reported the frequent detection of polyomaviruses (BK virus [BKV] or simian virus 40 [SV40]) in 46% of stool samples from hospitalized children. In order to determine if adults exhibit fecal shedding of polyomavirus, single stool specimens from healthy adults were evaluated by PCR. Overall, 20 (18.2%) of 110 specimens were positive for human polyomaviruses: 9 with BKV, 9 with JC virus (JCV), 1 with SV40, and 1 with both JCV and SV40. Among the 94 subjects without immune compromise, 17 (18.1%) were excreting polyomaviruses. This shedding frequency in adults was significantly lower than that observed in children (
P
< 0.001). These findings support the hypothesis that the gastrointestinal tract may be a site of polyomavirus persistence, and they suggest a fecal-oral route of viral transmission.
The CXCR4-Tropic Human Immunodeficiency Virus Envelope Promotes More-Efficient Gene Delivery to Resting CD4+T Cells than the Vesicular Stomatitis Virus Glycoprotein G Envelope
Authors: Agosto Luis M. , Yu Jianqing J. , Liszewski Megan K. , Baytop Clifford , Korokhov Nikolay , Humeau Laurent M. , O'Doherty Una 
Published: June 2009

ABSTRACTCurrent gene transfer protocols for resting CD4+T cells include an activation step to enhance transduction efficiency. This step is performed because it is thought that resting cells are resistant to transduction by lentiviral-based gene therapy vectors. However, activating resting cells prior to transduction alters their physiology, with foreseeable and unforeseeable negative consequences. Thus, it would be desirable to transduce resting CD4+T cells without activation. We recently demonstrated, contrary to the prevailing belief, that wild-type human immunodeficiency virus (HIV) integrates into resting CD4+T cells. Based on that finding, we investigated whether a commonly used, vesicular stomatitis virus glycoprotein G (VSV-G)-pseudotyped lentiviral gene therapy vector could also integrate into resting CD4+T cells. To investigate this, we inoculated resting CD4+T cells with lentiviral particles that were pseudotyped with VSV-G or CXCR4-tropic HIV Env and assayed binding, fusion, reverse transcription, and integration. We found that the VSV-G-pseudotyped lentiviral vector failed to fuse to resting CD4+T cells while HIV Env-pseudotyped lentiviral vectors fused, reverse transcribed, and integrated in resting cells. Our findings suggest that HIV Env could be used effectively for the delivery of therapeutic genes to resting CD4+T cells and suggest that fusion may be the critical step restricting transduction of resting CD4+T cells by lentiviral gene therapy vectors.
Simian Immunodeficiency Virus SIVrcm, a Unique CCR2-Tropic Virus, Selectively Depletes Memory CD4
+
T Cells in Pigtailed Macaques through Expanded Coreceptor Usage In Vivo
Authors: Gautam Rajeev , Gaufin Thaidra , Butler Isolde , Gautam Aarti , Barnes Mary , Mandell Daniel , Pattison Melissa , Tatum Coty , Macfarland Jeanne , Monjure Christopher , Marx Preston A. , Pandrea Ivona , Apetrei Cristian 
Published: June 2009

ABSTRACT

Simian immunodeficiency virus SIVrcm, which naturally infects red-capped mangabeys (RCMs), is the only SIV that uses CCR2 as its main coreceptor due to the high frequency of a CCR5 deletion in RCMs. We investigated the dynamics of SIVrcm infection to identify specific pathogenic mechanisms associated with this major difference in SIV biology. Four pigtailed macaques (PTMs) were infected with SIVrcm, and infection was monitored for over 2 years. The dynamics of in vivo SIVrcm replication in PTMs was similar to that of other pathogenic and nonpathogenic lymphotropic SIVs. Plasma viral loads (VLs) peaked at 10
7
to 10
9
SIVrcm RNA copies/ml by day 10 postinoculation (p.i.). A viral set point was established by day 42 p.i. at 10
3
to 10
5
SIVrcm RNA copies/ml and lasted up to day 180 p.i., when plasma VLs decreased below the threshold of detection, with blips of viral replication during the follow-up. Intestinal SIVrcm replication paralleled that of plasma VLs. Up to 80% of the CD4
+
T cells were depleted by day 28 p.i. in the gut. The most significant depletion (>90%) involved memory CD4
+
T cells. Partial CD4
+
T-cell restoration was observed in the intestine at later time points. Effector memory CD4
+
T cells were the least restored. SIVrcm strains isolated from acutely infected PTMs used CCR2 coreceptor, as reported, but expansion of coreceptor usage to CCR4 was also observed. Selective depletion of effector memory CD4
+
T cells is in contrast with predicted in vitro tropism of SIVrcm for macrophages and is probably due to expansion of coreceptor usage. Taken together, these findings emphasize the importance of understanding the selective forces driving viral adaptation to a new host.
Determinants of Hepatitis C Virus p7 Ion Channel Function and Drug Sensitivity Identified In Vitro
Authors: StGelais Corine , Foster Toshana L. , Verow Mark , Atkins Elizabeth , Fishwick Colin W. G. , Rowlands David , Harris Mark , Griffin Stephen 
Published: June 2009

ABSTRACT

Hepatitis C virus (HCV) chronically infects 170 million individuals, causing severe liver disease. Although antiviral chemotherapy exists, the current regimen is ineffective in 50% of cases due to high levels of innate virus resistance. New, virus-specific therapies are forthcoming although their development has been slow and they are few in number, driving the search for new drug targets. The HCV p7 protein forms an ion channel in vitro and is critical for the secretion of infectious virus. p7 displays sensitivity to several classes of compounds, making it an attractive drug target. We recently demonstrated that p7 compound sensitivity varies according to viral genotype, yet little is known of the residues within p7 responsible for channel activity or drug interactions. Here, we have employed a liposome-based assay for p7 channel function to investigate the genetic basis for compound sensitivity. We demonstrate using chimeric p7 proteins that neither the two
trans
-membrane helices nor the p7 basic loop individually determines compound sensitivity. Using point mutation analysis, we identify amino acids important for channel function and demonstrate that null mutants exert a dominant negative effect over wild-type protein. We show that, of the three hydrophilic regions within the amino-terminal
trans
-membrane helix, only the conserved histidine at position 17 is important for genotype 1b p7 channel activity. Mutations predicted to play a structural role affect both channel function and oligomerization kinetics. Lastly, we identify a region at the p7 carboxy terminus which may act as a specific sensitivity determinant for the drug amantadine.
Functional Characterization of Negri Bodies (NBs) in Rabies Virus-Infected Cells: Evidence that NBs Are Sites of Viral Transcription and Replication
Authors: Lahaye Xavier , Vidy Aurore , Pomier Carole , Obiang Linda , Harper Francis , Gaudin Yves , Blondel Danielle 
Published: June 2009

ABSTRACT
Rabies virus infection induces the formation of cytoplasmic inclusion bodies that resemble Negri bodies found in the cytoplasm of some infected nerve cells. We have studied the morphogenesis and the role of these Negri body-like structures (NBLs) during viral infection. The results indicate that these spherical structures (one or two per cell in the initial stage of infection), composed of the viral N and P proteins, grow during the virus cycle before appearing as smaller structures at late stages of infection. We have shown that the microtubule network is not necessary for the formation of these inclusion bodies but is involved in their dynamics. In contrast, the actin network does not play any detectable role in these processes. These inclusion bodies contain Hsp70 and ubiquitinylated proteins, but they are not misfolded protein aggregates. NBLs, in fact, appear to be functional structures involved in the viral life cycle. Specifically, using in situ fluorescent hybridization techniques, we show that all viral RNAs (genome, antigenome, and every mRNA) are located inside the inclusion bodies. Significantly, short-term RNA labeling in the presence of BrUTP strongly suggests that the NBLs are the sites where viral transcription and replication take place.
Introduction of Exogenous Epitopes in the Variable Regions of the Human Immunodeficiency Virus Type 1 Envelope Glycoprotein: Effect on Viral Infectivity and the Neutralization Phenotype
Authors: Wallace Aaron , Stamatatos Leonidas 
Published: June 2009

ABSTRACT
In this study we examined whether human immunodeficiency virus type 1 (HIV-1) is equally susceptible to neutralization by a given antibody when the epitope of this antibody is introduced at different positions within the viral envelope glycoprotein (Env). To this end, we introduced two exogenous “epitope tags” at different locations within three major Env regions in two distinct HIV-1 isolates. We examined how the introduction of the exogenous epitopes affects Env expression, Env incorporation into virions, Env fusogenic potential, and viral susceptibility to neutralization. Our data indicate that even within the same Env region, the exact positioning of the epitope impacts the susceptibility of the virus to neutralization by the antibody that binds to that epitope. Our data also indicate that even if the same epitope is introduced in the exact same position on two different Envs, its exposure and, as a result, the neutralization susceptibility of the virus, can be very different. In contrast to the findings of previous studies conducted with HIV-1 isolates other than those used here, but in agreement with results obtained with simian immunodeficiency virus, we observed that tagging of the fourth variable region of Env (V4) did not result in neutralization by the anti-tag antibodies. Our data indicate that epitopes in V4 are not properly exposed within the functional HIV-1 trimeric Env spike, suggesting that V4 may not be a good target for vaccine-elicited neutralizing antibodies.
Truncation of TRIM5 in the
Feliformia
Explains the Absence of Retroviral Restriction in Cells of the Domestic Cat
Authors: McEwan William A. , Schaller Torsten , Ylinen Laura M. , Hosie Margaret J. , Towers Greg J. , Willett Brian J. 
Published: June 2009

ABSTRACT

TRIM5α mediates a potent retroviral restriction phenotype in diverse mammalian species. Here, we identify a TRIM5 transcript in cat cells with a truncated B30.2 capsid binding domain and ablated restrictive function which, remarkably, is conserved across the
Feliformia
. Cat TRIM5 displayed no restriction activity, but ectopic expression conferred a dominant negative effect against human TRIM5α. Our findings explain the absence of retroviral restriction in cat cells and suggest that disruption of the TRIM5 locus has arisen independently at least twice in the
Carnivora
, with implications concerning the evolution of the host and pathogen in this taxon.
Population-based estimates of injuries in Sri Lanka
Authors: Navaratne K V , Fonseka P , Rajapakshe L , Somatunga L , Ameratunga S , Ivers R , Dandona R 
Published: June 2009

Background:Injuries are the leading cause of public hospital admission in Sri Lanka. Data on injury epidemiology to plan prevention programmes to reduce injury burden are not readily available.Objectives:To assess the incidence of various types of injuries in the Galle district, Sri Lanka.Methods:9568 individuals of all ages were selected from 2000 households in a population-based cross-sectional survey using a stratified cluster sampling technique. Data on non-fatal injuries in the last 30 days irrespective of severity, fatal injuries and those that resulted in disability in the last 12 months were documented. Proxy data were used for half of the injury cases.Results:195 (2%) individuals reported non-fatal injuries during the last 30 days, giving an age-sex-urban-rural adjusted annual incidence of 24.6 per 100 population. The leading causes of non-fatal injuries were falls (adjusted annual incidence 6.7 per 100 population, 95% CI 6.0 to 7.3) and mechanical injuries (6.3; 95% CI 5.7 to 6.8), followed by road traffic injuries (4.9; 95% CI 4.4 to 5.5). 114 (58.5%) individuals needed outpatient care and 50 (25.6%) needed inpatient care for their injuries. The annual injury mortality rate and disability rate were 177 (95% CI 72 to 283) and 290 (95% CI 250 to 330) per 100 000 population, respectively.Conclusions:Nearly one in four people reported non-fatal injury; the majority sought medical attention in this population. It is important to utilise injury epidemiology to develop and implement interventions to reduce the burden of injuries in the population and on the hospitals in Sri Lanka.
Neighbourhood income gradients in hospitalisations due to motor vehicle traffic incidents among Canadian children
Authors: Oliver L , Kohen D 
Published: June 2009

Objective:To investigate income gradients in motor vehicle traffic injury hospitalisation for vehicle occupants and pedestrians/cyclists among children in urban and rural Canada.Design:Four years (2001/02–2004/05) of acute-care hospitalisation discharge records for children aged 0–19 years were analysed. International Classification of Disease codes were used to determine hospitalisations due to motor vehicle traffic incidents for occupants and pedestrians/cyclists. Rates of injury (per 10 000 person years) were calculated by neighbourhood income quintiles for urban and rural areas.Results:Among children (0–19 years), rates of vehicle occupant hospitalisation were higher in rural (5.07, 95% CI 4.90 to 5.25) than urban areas (2.08, 95% CI 2.03 to 2.14). In rural areas, children from lower income neighbourhoods had higher vehicle occupant hospitalisation rates than those from the richest neighbourhoods (5.52, 95% CI 5.13 to 5.93 vs 4.30, 95% CI 3.97 to 4.66). In urban areas vehicle occupant hospitalisation rates were similar among children from the poorest and richest neighbourhoods—but higher among children from middle income neighbourhoods. In urban areas, but not rural areas, the hospitalisation rate for pedestrians/cyclists systematically increased with decreasing neighbourhood income. In urban areas the pedestrian/cyclist hospitalisation rate was four times higher for children from the poorest (1.40, 95% CI 1.25 to 1.57) than from the richest (0.34, 95% CI 0.28 to 0.43) neighbourhoods.Conclusions:While vehicle occupant and pedestrian/cyclist motor vehicle traffic injuries are more frequent among children from lower income neighbourhoods, gradients are most pronounced for pedestrians/cyclists in urban areas.
Causes of injuries resulting in hospitalisation in Australia: assessing coder agreement on external causes
Authors: McKenzie K , Enraght-Moony E L , Waller G , Walker S M , Harrison J E , McClure R J 
Published: June 2009

Objective:To assess extent of coder agreement for external causes of injury using ICD-10-AM for injury-related hospitalisations in Australian public hospitals.Methods:A random sample of 4850 discharges from 2002 to 2004 was obtained from a stratified random sample of 50 hospitals across four states in Australia. On-site medical record reviews were conducted and external cause codes were assigned blinded to the original coded data. Code agreement levels were grouped into the following agreement categories: block level, 3-character level, 4-character level, 5th-character level, and complete code level.Results:At a broad block level, code agreement was found in over 90% of cases for most mechanisms (eg, transport, fall). Percentage disagreement was 26.0% at the 3-character level; agreement for the complete external cause code was 67.6%. For activity codes, the percentage of disagreement at the 3-character level was 7.3% and agreement for the complete activity code was 68.0%. For place of occurrence codes, the percentage of disagreement at the 4-character level was 22.0%; agreement for the complete place code was 75.4%.Conclusions:With 68% agreement for complete codes and 74% agreement for 3-character codes, as well as variability in agreement levels across different code blocks, place and activity codes, researchers need to be aware of the reliability of their specific data of interest when they wish to undertake trend analyses or case selection for specific causes of interest.
White Adipose Tissue Cells Are Recruited by Experimental Tumors and Promote Cancer Progression in Mouse Models
Authors: Zhang Yan , Daquinag Alexes , Traktuev Dmitry O. , Amaya-Manzanares Felipe , Simmons Paul J. , March Keith L. , Pasqualini Renata , Arap Wadih , Kolonin Mikhail G. 
Published: June 2009

Abstract
The connection between obesity and accelerated cancer progression has been established, but the mediating mechanisms are not well understood. We have shown that stromal cells from white adipose tissue (WAT) cooperate with the endothelium to promote blood vessel formation through the secretion of soluble trophic factors. Here, we hypothesize that WAT directly mediates cancer progression by serving as a source of cells that migrate to tumors and promote neovascularization. To test this hypothesis, we have evaluated the recruitment of WAT-derived cells by tumors and the effect of their engraftment on tumor growth by integrating a transgenic mouse strain engineered for expansion of traceable cells with established allograft and xenograft cancer models. Our studies show that entry of adipose stromal and endothelial cells into systemic circulation leads to their homing to and engraftment into tumor stroma and vasculature, respectively. We show that recruitment of adipose stromal cells by tumors is sufficient to promote tumor growth. Finally, we show that migration of stromal and vascular progenitor cells from WAT grafts to tumors is also associated with acceleration of cancer progression. These results provide a biological insight for the clinical association between obesity and cancer, thus outlining potential avenues for preventive and therapeutic strategies. [Cancer Res 2009;69(12):5259–66]
Loss of Retinal Cadherin Facilitates Mammary Tumor Progression and Metastasis
Authors: Agiostratidou Georgia , Li Maomi , Suyama Kimita , Badano Ines , Keren Rinat , Chung Su , Anzovino Amy , Hulit James , Qian Binzhi , Bouzahzah Boumediene , Eugenin Eliseo , Loudig Olivier , Phillips Greg R. , Locker Joseph , Hazan Rachel B. 
Published: June 2009

Abstract
The mammary epithelium is thought to be stabilized by cell-cell adhesion mediated mainly by E-cadherin (E-cad). Here, we show that another cadherin, retinal cadherin (R-cad), is critical for maintenance of the epithelial phenotype. R-cad is expressed in nontransformed mammary epithelium but absent from tumorigenic cell lines. In vivo, R-cad was prominently expressed in the epithelium of both ducts and lobules. In human breast cancer, R-cad was down-regulated with tumor progression, with high expression in ductal carcinoma in situ and reduced expression in invasive duct carcinomas. By comparison, E-cad expression persisted in invasive breast tumors and cell lines where R-cad was lost. Consistent with these findings, R-cad knockdown in normal mammary epithelium stimulated invasiveness and disrupted formation of acini despite continued E-cad expression. Conversely, R-cad overexpression in aggressive cell lines induced glandular morphogenesis and inhibited invasiveness, tumor formation, and lung colonization. R-cad also suppressed the matrix metalloproteinase 1 (MMP1), MMP2, and cyclooxygenase 2 gene expression associated with pulmonary metastasis. The data suggest that R-cad is an adhesion molecule of the mammary epithelium, which acts as a critical regulator of the normal phenotype. As a result, R-cad loss contributes to epithelial suppression and metastatic progression. [Cancer Res 2009;69(12):5030–8]