bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validation of an Enzyme-Linked Immunosorbent Assay for Diagnosis of Human Trichinellosis
Authors: Gómez-Morales Maria Angeles , Ludovisi Alessandra , Amati Marco , Cherchi Simona , Pezzotti Patrizio , Pozio Edoardo 
Published: October 2008

ABSTRACT

Trichinellosis is a zoonotic disease caused by the consumption of raw or semiraw meat from different animals harboring
Trichinella
larvae in their muscles. Since there are no pathognomonic signs, diagnosis can be difficult; for this reason, serology is important. The objective of this study was to validate an enzyme-linked immunosorbent assay (ELISA) using excretory/secretory antigens to detect anti-
Trichinella
immunoglobulin G antibodies in human sera. A total of 3,505 human serum samples were tested. A receiver-operator characteristic (ROC) curve analysis was performed. The accuracy of the test was determined by calculating the area under the curve, which was equal to 0.999, indicating high accuracy. The coefficient of variation calculated for data from four serum samples in eight working sessions was no higher than 5% for the positive sera or 14% for the negative sera. Moreover, the analysis of the differences in optical density between duplicates indicated a high repeatability for the ELISA. At the ROC optimized cutoff, the sensitivity and specificity of the test were, respectively, 99.2% and 90.6% (specificity of 95.6% when excluding the samples from multiparasitized persons from Tanzania). The validated ELISA showed good performance in terms of sensitivity, repeatability, and reproducibility, whereas the specificity was limited. These results suggest that this test is suitable for detecting anti-
Trichinella
antibodies in human sera for diagnostic purposes, whereas its use in epidemiological surveys could be questionable.
Assessment of Three Commercially Available Serologic Assays for Detection of Antibodies to
Mycobacterium tuberculosis
and Identification of Active Tuberculosis
Authors: Anderson Brian L. , Welch Ryan J. , Litwin Christine M. 
Published: October 2008

ABSTRACT

Tuberculosis (TB) caused by
Mycobacterium tuberculosis
remains a major world disease, with approximately 9 million new cases each year. Identification and treatment of active disease are essential for TB control. Serology may offer increased detection of active disease in patients with a positive tuberculin skin test (TST) or QuantiFERON-TB (QFT-G). The InBios Active Tb
Detect
immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA), IBL
M. tuberculosis
IgG ELISA, and Anda Biologics TB ELISAs were evaluated for the ability to detect
M. tuberculosis
antibodies in patients with active disease. Agreement, sensitivity, and specificity for each ELISA were determined and compared to those for culture or amplified direct detection and
M. tuberculosis
low-risk control patients. The InBios Active Tb
Detect
ELISA had an agreement of 96.2%, a sensitivity of 83.3%, and a specificity of 98.9%. The IBL
M. tuberculosis
ELISA had an agreement of 84.0%, a sensitivity of 5.6%, and a specificity of 100.0%. The agreement, sensitivity, and specificity of the Anda Biologics TB ELISA were 74.2%, 83.3%, and 72.0%, respectively. The sensitivity for detecting
M. tuberculosis
antibodies in human immunodeficiency virus-associated TB was 50% for both the InBios Active Tb
Detect
ELISA and the Anda Biologics TB ELISA and 0% for the IBL
M. tuberculosis
ELISA. The positivity rates for InBios Active Tb
Detect
ELISA, IBL
M. tuberculosis
ELISA, and Anda Biologics TB ELISA in latently infected individuals positive by TST and/or QFT-G were 5.1%, 0.0%, and 30.8%, respectively. It can be concluded that the InBios Active Tb
Detect
IgG ELISA is superior to the other ELISAs in accurately detecting active TB.
Seroprevalence of Antibodies against Serogroup C Meningococci in England in the Postvaccination Era
Authors: Trotter Caroline L. , Borrow Ray , Findlow Jamie , Holland Ann , Frankland Sarah , Andrews Nick J. , Miller Elizabeth 
Published: October 2008

ABSTRACT

The United Kingdom introduced meningococcal serogroup C conjugate (MCC) vaccines in 1999, resulting in substantial declines in serogroup C disease and carriage. Here, we measured the age-specific prevalence of serum bactericidal antibodies (SBA) to
Neisseria meningitidis
serogroup C and immunoglobulin G (IgG) concentrations to serogroups A, C, W-135, and Y in 2,673 serum samples collected in England between 2000 and 2004. We compared the seroprevalence of SBA titers of ≥8 in the postvaccination era with results from an earlier prevaccination study conducted using the same methods. We found that the percentages of individuals with protective SBA titers were higher in 2000 to 2004 in all of the age groups targeted for MCC vaccination. In the postvaccine era, the prevalence of protective titers was high (75%) in children who had recently been offered routine immunization, but this fell to 36% more than 18 months after scheduled immunization. In the cohorts targeted in the catch-up campaign, the percentage achieving SBA titers of ≥8 was higher in children offered the vaccine at ages 5 to 17 years than in children offered the vaccine at ages 1 to 4 years. The geometric mean concentration (GMC) IgG for serogroup C followed a similar pattern, corresponding to the age at and time since scheduled MCC vaccination. Serogroup-specific IgG GMCs for W-135 and Y were low and showed little variation by age. Serogroup A IgG GMCs were higher, possibly reflecting exposure to cross-reacting antigens. Although the incidence of serogroup C disease remains low due to persisting herd effects, population antibody levels to serogroup C meningococci should be monitored so that potentially susceptible age groups can be identified should herd immunity wane.
Orally Administered
Mycobacterium vaccae
Modulates Expression of Immunoregulatory Molecules in BALB/c Mice with Pulmonary Tuberculosis
Authors: Hernández-Pando Rogelio , Aguilar Diana , Orozco Hector , Cortez Yuriria , Brunet Laura Rosa , Rook Graham A. 
Published: October 2008

ABSTRACT

The environmental saprophyte
Mycobacterium vaccae
induces a Th1 response and cytotoxic T cells that recognize
M. tuberculosis
, and by subcutaneous injection, it is therapeutic for pulmonary tuberculosis (TB) induced by high-dose challenge in BALB/c mice. However,
M. vaccae
also drives regulatory T cells that inhibit Th2 responses, and this is seen in allergy models, not only following subcutaneous injection but also after oral administration. An oral immunotherapeutic for TB would be clinically useful, so we investigated
M. vaccae
given orally by gavage at 28-day intervals in the TB model. We used two different protocols: starting the oral
M. vaccae
either 1 day before or 32 days after infection with
M. tuberculosis
. Throughout the infection (until 120 days), we monitored outcome (CFU), molecules involved in the development of immunoregulation (Foxp3, hemoxygenase 1, idoleamine 2,3-dioxygenase, and transforming growth factor β [TGF-β]), and indicators of cytokine balance (tumor necrosis factor, inducible nitric oxide synthase, interleukin-4 [IL-4], and IL-4δ2; an inhibitory splice variant of IL-4 associated with improved outcome in human TB). Oral
M. vaccae
had a significant effect on CFU and led to increased expression of Th1 markers and of IL-4δ2, while suppressing IL-4, Foxp3, and TGF-β. When administered 1 day before infection, oral
M. vaccae
induced a striking peak of expression of hemoxygenase 1. In conclusion, we show novel information about the expression in TB of murine IL-4δ2 and molecules involved in immunoregulation and show that these can be modulated by oral administration of a saprophytic mycobacterium. A clinical trial of oral
M. vaccae
in extensively drug-resistant TB might be justified.
Cigarette fires and burns in a population of New Zealand smokers
Authors: Smith J , Bullen C , Laugesen M , Glover M 
Published: October 2008

Objectives:To identify the proportion of adult cigarette smokers who have experienced cigarette-caused fires and burns and to describe smoker characteristics associated with increased risk of cigarette-caused fires and burns.Methods:Data on cigarette-caused fires and burns were collected in the baseline questionnaire of a randomised trial of a smoking cessation intervention conducted in New Zealand between March 2006 and May 2007. Participants were adult callers to a national smoking cessation counselling service. Lifetime prevalence estimates of cigarette-caused fires and burns were obtained and associations between smoker characteristics and risk of fires and burns examined using logistic regression.Results:Of 1097 participants in the trial at baseline, 75 (6.8%) reported past experience of ⩾1 fires caused by cigarettes (96 fires reported in total) and 658 (60.0%) described at least 1 cigarette-caused burn. In all, 57 participants (5.2%) reported burns that required medical attention. Male sex and Māori ethnicity (indigenous New Zealanders, who comprise 15% of the national population and among whom 42% of adults are smokers) were associated with increased risk of cigarette-caused fires. Male sex, younger age, younger age of smoking initiation, being unmarried, having a partner who smoked, having a higher education level and an annual income of $20 000 or more were associated with increased risk of cigarette burn injuries.Conclusions:The results indicate that cigarette-caused fires and burns are common among New Zealand smokers, are a source of inequality and therefore deserve greater attention from health advocates and policymakers.
How does increasingly plainer cigarette packaging influence adult smokers’ perceptions about brand image? An experimental study
Authors: Wakefield M A , Germain D , Durkin S J 
Published: October 2008

Background:Cigarette packaging is a key marketing strategy for promoting brand image. Plain packaging has been proposed to limit brand image, but tobacco companies would resist removal of branding design elements.Method:A 3 (brand types) × 4 (degree of plain packaging) between-subject experimental design was used, using an internet online method, to expose 813 adult Australian smokers to one randomly selected cigarette pack, after which respondents completed ratings of the pack.Results:Compared with current cigarette packs with full branding, cigarette packs that displayed progressively fewer branding design elements were perceived increasingly unfavourably in terms of smokers’ appraisals of the packs, the smokers who might smoke such packs, and the inferred experience of smoking a cigarette from these packs. For example, cardboard brown packs with the number of enclosed cigarettes displayed on the front of the pack and featuring only the brand name in small standard font at the bottom of the pack face were rated as significantly less attractive and popular than original branded packs. Smokers of these plain packs were rated as significantly less trendy/stylish, less sociable/outgoing and less mature than smokers of the original pack. Compared with original packs, smokers inferred that cigarettes from these plain packs would be less rich in tobacco, less satisfying and of lower quality tobacco.Conclusion:Plain packaging policies that remove most brand design elements are likely to be most successful in removing cigarette brand image associations.
Regulation of Estrogenic Effects by Beclin 1 in Breast Cancer Cells
Authors: John Shali , Nayvelt Irina , Hsu Hui-Chen , Yang PingAr , Liu Wensheng , Das Gokul M. , Thomas Thresia , Thomas T.J. 
Published: October 2008

Abstract
Beclin 1 is an essential mediator of autophagy and a regulator of cell growth and cell death. We examined the effect of Beclin 1 overexpression on the action of estradiol (E2) and two antiestrogens, raloxifene and 4-hydroxytamoxifen, in estrogen receptor α (ERα)-positive MCF-7 breast cancer cells. [3H]-thymidine incorporation studies showed that Beclin 1–overexpressing cells (MCF-7.beclin) had a lower proliferative response to E2 compared with cells transfected with vector control (MCF-7.control). There was only a 35% increase in [3H]-thymidine incorporation, after 24 hours of E2 treatment of MCF-7.beclin cells compared with untreated cells, whereas this increase was 2-fold for MCF-7.control cells. E2-induced changes in the expression of early-response genes were examined by real-time quantitiative PCR. There were significant differences in the pattern of expression of E2-induced genes c-myc, c-fos, Erg-1, and Nur77 between MCF-7.beclin and MCF-7.control cells two hours after treatment. Although E2-induced growth of MCF-7.control cells was completely inhibited by 500 nmol/L raloxifene or 500 nmol/L 4-hydroxytamoxifen, these concentrations of antiestrogens had no significant effect on the growth of MCF-7.beclin cells. Confocal microscopic and coimmunoprecipitation studies showed evidence for colocalization and association of Beclin 1 and ERα. In addition, E2 caused a decrease in Akt phosphorylation in MCF-7.beclin cells, compared with a 3-fold increase in MCF-7 cells, five minutes after treatment. These results indicate that Beclin 1 can down-regulate estrogenic signaling and growth response, and contribute to the development of antiestrogen resistance. This observation might be useful to define and overcome antiestrogen resistance of breast cancer. [Cancer Res 2008;68(19):7855–63]
The Polycomb Gene Product BMI1 Contributes to the Maintenance of Tumor-Initiating Side Population Cells in Hepatocellular Carcinoma
Authors: Chiba Tetsuhiro , Miyagi Satoru , Saraya Atsunori , Aoki Ryutaro , Seki Atsuyoshi , Morita Yohei , Yonemitsu Yutaka , Yokosuka Osamu , Taniguchi Hideki , Nakauchi Hiromitsu , Iwama Atsushi 
Published: October 2008

AbstractSide population (SP) cell analysis and sorting have been successfully applied to hepatocellular carcinoma (HCC) cell lines to identify a minor cell population with cancer stem cell properties. However, the molecular mechanisms operating in SP cells remain unclear. The polycomb gene product BMI1 plays a central role in the self-renewal of somatic stem cells in a variety of tissues and organs and seems to be implicated in tumor development. In this study, we determined the critical role of BMI1 in the maintenance of cancer stem cells with the SP phenotype in HCC cell lines. BMI1 was preferentially expressed in SP cells in Huh7 and PLC/PRF/5 HCC cells compared with the corresponding non-SP cells. Lentiviral knockdown of BMI1 considerably decreased the number of SP cells in both Huh7 and PLC/PRF/5 cells. Long-term culture of purified SP cells resulted in a drastic reduction in the SP subpopulation upon the BMI1 knockdown, indicating that BMI1 is required for the self-renewal of SP cells in culture. More importantly, the BMI1 knockdown abolished the tumor-initiating ability of SP cells in nonobese diabetic/severe combined immunodeficiency mice. Derepression of the INK4A and ARF genes that are major targets for BMI1 was not necessarily associated with impaired self-renewal of SP cells caused by BMI1 knockdown. In conclusion, our findings define an important role for BMI1 in the maintenance of tumor-initiating SP cells in HCC. BMI1 might be a novel therapeutic target for the eradication of cancer stem cells in HCC. [Cancer Res 2008;68(19):7742–9]
A Bicistronic CYCLIN D1-TROP2 mRNA Chimera Demonstrates a Novel Oncogenic Mechanism in Human Cancer
Authors: Guerra Emanuela , Trerotola Marco , Dell' Arciprete Roberta , Bonasera Veronica , Palombo Barbara , El-Sewedy Tarek , Ciccimarra Tommaso , Crescenzi Carlo , Lorenzini Franco , Rossi Cosmo , Vacca Giovanna , Lattanzio Rossano , Piantelli Mauro , Alberti Saverio 
Published: October 2008

Abstract
A chimeric CYCLIN D1-TROP2 mRNA was isolated from human ovarian and mammary cancer cells. The CYCLIN D1-TROP2 mRNA was shown to be a potent oncogene as it transforms naïve, primary cells in vitro and induces aggressive tumor growth in vivo in cooperation with activated RAS. Silencing of the chimeric mRNA inhibits the growth of breast cancer cells. The CYCLIN D1-TROP2 mRNA was expressed by a large fraction of the human gastrointestinal, ovarian, and endometrial tumors analyzed. It is most frequently detected in intestinal cell aneuploid cancers and it is coexpressed with activated RAS oncogenes, consistent with a cooperative transforming activity in human cancers. The chimeric mRNA is a bicistronic transcript of post transcriptional origin that independently translates the Cyclin D1 and Trop-2 proteins. This is a novel mechanism of CYCLIN D1 activation that achieves the truncation of the CYCLIN D1 mRNA in the absence of chromosomal rearrangements. This leads to a higher CYCLIN D1 mRNA stability, with inappropriate expression during the cell cycle. The stabilized CYCLIN D1 mRNA cooperates with TROP2 in stimulating the growth of the expressing cells. These findings show a novel epigenetic, oncogenic mechanism, which seems to be widespread in human cancers. [Cancer Res 2008;68(19):8113–21]
Senescence-Associated Exosome Release from Human Prostate Cancer Cells
Authors: Lehmann Brian D. , Paine Matthew S. , Brooks Adam M. , McCubrey James A. , Renegar Randall H. , Wang Rong , Terrian David M. 
Published: October 2008

Abstract
Males of advanced age represent a rapidly growing population at risk for prostate cancer. In the contemporary setting of earlier detection, a majority of prostate carcinomas are still clinically localized and often treated using radiation therapy. Our recent studies have shown that premature cellular senescence, rather than apoptosis, accounts for most of the clonogenic death induced by clinically relevant doses of irradiation in prostate cancer cells. We show here that this treatment-induced senescence was associated with a significantly increased release of exosome-like microvesicles. In premature senescence, this novel secretory phenotype was dependent on the activation of p53. In addition, the release of exosome-like microvesicles also increased during proliferative senescence in normal human diploid fibroblasts. These data support the hypothesis that senescence, initiated either by telomere attrition (e.g., aging) or DNA damage (e.g., radiotherapy), may induce a p53-dependent increase in the biogenesis of exosome-like vesicles. Ultrastructural analysis and RNA interference–mediated knockdown of Tsg101 provided significant evidence that the additional exosomes released by prematurely senescent prostate cancer cells were principally derived from multivesicular endosomes. Moreover, these exosomes were enriched in B7-H3 protein, a recently identified diagnostic marker for prostate cancer, and an abundance of what has recently been termed “exosomal shuttle RNA.” Our findings are consistent with the proposal that exosomes can transfer cargos, with both immunoregulatory potential and genetic information, between cells through a novel mechanism that may be recruited to increase exosome release during accelerated and replicative cellular senescence. [Cancer Res 2008;68(19):7864–71]
SCL/TAL1 Interrupting Locus Derepresses GLI1 from the Negative Control of Suppressor-of-Fused in Pancreatic Cancer Cell
Authors: Kasai Kenji , Inaguma Shingo , Yoneyama Akiko , Yoshikawa Kazuhiro , Ikeda Hiroshi 
Published: October 2008

Abstract
As a physically binding protein of GLI1 transcription factor, Suppressor-of-Fused (SUFU) has been placed in the center of negative regulation of Hedgehog (Hh) signaling. SUFU tethers GLI1 in cytoplasm, and in some circumstances, it moves into the nucleus in association with GLI1, leading to the suppression of GLI1 target gene expression by recruiting a corepressor complex. The activated transcriptional function of GLI1 is important for cellular proliferation in a variety of human cancers. However, it has not been revealed how GLI1 is derepressed from SUFU-mediated suppression. Here, we show SCL/TAL1 interrupting locus (SIL) product, a cytoplasmic protein overexpressed in pancreatic ductal adenocarcinoma (PDA), is responsible for the derepression of GLI1. We found SIL associated with the carboxyl terminus of SUFU, one of two distinct GLI1-binding domains, and this association was responsible for cytoplasmic tethering of SUFU. Overexpressed SIL attenuated SUFU-mediated cytoplasmic tethering and target gene suppression of GLI1. Knockdown of SIL in PDA cells conversely induced the nuclear accumulation of SUFU in association with GLI1 and the transcriptional suppression of GLI1 target genes. Importantly, we also showed that oncogenic K-RAS, and not Sonic hedgehog, enhanced the SIL association with the amino-terminus of SUFU, the other GLI1-binding domain that led to further increase of nuclear translocation of GLI1. These results uncover the role of SIL in derepressing GLI1 from the negative control of SUFU, which is a crucial step for activating Hh signaling in cancer cells. [Cancer Res 2008;68(19):7723–9]
Prostaglandin E2 Regulates Tumor Angiogenesis in Prostate Cancer
Authors: Jain Shalini , Chakraborty Goutam , Raja Remya , Kale Smita , Kundu Gopal C. 
Published: October 2008

AbstractIn cancer management, the cyclooxygenase (COX)–targeted approach has shown great promise in anticancer therapeutics. However, the use of COX-2 inhibitors has side effects and health hazards; thus, targeting its major metabolite prostaglandin E2 (PGE2)–mediated signaling pathway might be a rational approach for the next generation of cancer management. Recent studies on several in vitro and in vivo models have revealed that elevated expression of COX-2 correlates with prostate tumor growth and angiogenesis. In this study, we have shown the in-depth molecular mechanism and the PGE2 activation of the epidermal growth factor receptor and β3 integrin through E prostanoid 2 (EP2)–mediated and EP4-mediated pathways, which lead to activator protein-1 (AP-1) activation. Moreover, PGE2 also induces activating transcription factor-4 (ATF-4) activation and stimulates cross-talk between ATF-4 and AP-1, which is unidirectional toward AP-1, which leads to the increased expressions of urokinase-type plasminogen activator and vascular endothelial growth factor and, eventually, regulates prostate tumor cell motility. In vivo Matrigel angiogenesis assay data revealed that PGE2 induces angiogenesis through EP2 and EP4. Human prostate cancer specimen analysis also supported our in vitro and in vivo studies. Our data suggest that targeting PGE2 signaling pathway (i.e., blocking EP2 and EP4 receptors) might be a rational therapeutic approach for overcoming the side effects of COX-2 inhibitors and that this might be a novel strategy for the next generation of prostate cancer management. [Cancer Res 2008;68(19):7750–9]