bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sampling 'hard-to-reach' populations in health research: yield from a study targeting Americans living in Canada
Authors: Southern Danielle A , Lewis Steven , Maxwell Colleen J , Dunn James R , Noseworthy Tom W , Corbett Gail , Thomas Karen , Ghali William A 
Published: August 2008

Abstract

Background
Some populations targeted in survey research can be hard to reach, either because of lack of contact information, or non-existent databases to inform sampling. Here, we present a methodological "case-report" of the yield of a multi-step survey study assessing views on health care among American emigres to Canada, a hard-to-reach population.

Methods
To sample this hard-to-reach population, we held a live media conference, supplemented by a nation-wide media release announcing the study. We prepared an 'op-ed' piece describing the study and how to participate. We paid for advertisements in 6 newspapers. We sent the survey information to targeted organizations. And lastly, we asked those who completed the web survey to send the information to others. We use descriptive statistics to document the method's yield.

Results
The combined media strategies led to 4 television news interviews, 10 newspaper stories, 1 editorial and 2 radio interviews. 458 unique individuals accessed the on-line survey, among whom 310 eligible subjects provided responses to the key study questions. Fifty-six percent reported that they became aware of the survey via media outlets, 26% by word of mouth, and 9% through both the media and word of mouth.

Conclusion
Our multi-step communication method yielded a sufficient sample of Americans living in Canada. This combination of paid and unpaid media exposure can be considered by others as a unique methodological approach to identifying and sampling hard-to-reach populations.
DNA methylation patterns in bladder cancer and washing cell sediments: a perspective for tumor recurrence detection
Authors: Negraes Priscilla D , Favaro Francine P , Camargo João Lauro V , Oliveira Maria Luiza CS , Goldberg José , Rainho Cláudia A , Salvadori Daisy MF 
Published: August 2008

Abstract

Background
Epigenetic alterations are a hallmark of human cancer. In this study, we aimed to investigate whether aberrant DNA methylation of cancer-associated genes is related to urinary bladder cancer recurrence.

Methods
A set of 4 genes, including CDH1 (E-cadherin), SFN (stratifin), RARB (retinoic acid receptor, beta) and RASSF1A (Ras association (RalGDS/AF-6) domain family 1), had their methylation patterns evaluated by MSP (Methylation-Specific Polymerase Chain Reaction) analysis in 49 fresh urinary bladder carcinoma tissues (including 14 cases paired with adjacent normal bladder epithelium, 3 squamous cell carcinomas and 2 adenocarcinomas) and 24 cell sediment samples from bladder washings of patients classified as cancer-free by cytological analysis (control group). A third set of samples included 39 archived tumor fragments and 23 matched washouts from 20 urinary bladder cancer patients in post-surgical monitoring. After genomic DNA isolation and sodium bisulfite modification, methylation patterns were determined and correlated with standard clinic-histopathological parameters.

Results

CDH1 and SFN genes were methylated at high frequencies in bladder cancer as well as in paired normal adjacent tissue and exfoliated cells from cancer-free patients. Although no statistically significant differences were found between RARB and RASSF1A methylation and the clinical and histopathological parameters in bladder cancer, a sensitivity of 95% and a specificity of 71% were observed for RARB methylation (Fisher's Exact test (p < 0.0001; OR = 48.89) and, 58% and 17% (p < 0.05; OR = 0.29) for RASSF1A gene, respectively, in relation to the control group.

Conclusion
Indistinct DNA hypermethylation of CDH1 and SFN genes between tumoral and normal urinary bladder samples suggests that these epigenetic features are not suitable biomarkers for urinary bladder cancer. However, RARB and RASSF1A gene methylation appears to be an initial event in urinary bladder carcinogenesis and should be considered as defining a panel of differentially methylated genes in this neoplasia in order to maximize the diagnostic coverage of epigenetic markers, especially in studies aiming at early recurrence detection.
Identification of a novel CHEK2variant and assessment of its contribution to the risk of breast cancer in French Canadian women
Authors: Novak David J , Chen Long Qi , Ghadirian Parviz , Hamel Nancy , Zhang Phil , Rossiny Vanessa , Cardinal Guy , Robidoux André , Tonin Patricia N , Rousseau Francois , Narod Steven A , Foulkes William D 
Published: August 2008

AbstractBackgroundBRCA1andBRCA2account for the majority of the known familial breast cancer risk, however, the impact of other cancer susceptibility genes largely remains to be elucidated. Checkpoint Kinase 2 (CHEK2) is an important signal transducer of cellular responses to DNA damage, whose defects have been associated with an increase in breast cancer risk. Previous studies have identified low penetranceCHEK2alleles such as 1100delC and I157T, as well as variants such as S428F in the Ashkenazi Jewish population and IVS2 + 1G>A in the Polish population. No founder allele has been specifically identified in the French Canadian population.MethodsThe 14 coding exons ofCHEK2were fully sequenced for variant alleles in a panel of 25 affected French Canadian women and 25 healthy controls. Two variants were identified of which one novel variant was further screened for in an additional panel of 667 breast cancer patients and 6548 healthy controls. Additional genotyping was conducted using allele specific PCR and a restriction digest assay. Significance of amino acid substitutions were deduced by employing comparative analysis techniques.ResultsTwo variants were identified: the previously reported silent substitution 252A>G (E84E) and the novel missense variant, 1217G>A (R406H). No significant difference in allele distribution between French Canadian women with breast cancer and healthy controls was observed (3/692, 0.43% vs. 22/6573, 0.33%, respectively, P = 0.73).ConclusionThe novel CHEK2 missense variant identified in this study, R406H, is unlikely to contribute to breast cancer risk in French Canadian women.
Fitness, motor competence and body composition as correlates of adolescent neck/shoulder pain: an exploratory cross-sectional study
Authors: Perry Mark C , Straker Leon M , O'Sullivan Peter B , Smith Anne J , Hands Beth 
Published: August 2008

AbstractBackgroundAdolescent neck/shoulder pain (NSP) is a common and sometimes debilitating problem. Several risk factors for this condition have been investigated, but no studies have previously evaluated associations between fitness, motor competence, body composition and adolescent NSP.Methods1608 males and females of mean age 14 years answered questions on their history of NSP (4 measures), and were tested for aerobic fitness, upper and lower limb power, trunk endurance, grip strength, shoulder flexibility, motor competence and anthropometric factors. Univariate and multivariate logistic regressions were used to test for associations between NSP and physical variables.ResultsThere were significant gender differences for most physical and pain variables. After multivariate analysis, males had lower odds of NSP if they had reduced back endurance [OR: 0.66 (95% CI: 0.46–0.97)], reduced persistent control [0.42 (0.19–0.95], and increased muscle power [0.33 (0.12–0.94)], and higher odds of NSP if they had a higher basketball throw [2.47 (1.22–5.00)] and jump performance [3.47 (1.55–7.74)]. Females had lower odds for NSP if they had a reduced jump performance [0.61(0.41–0.92)], a better basketball throw [0.60(0.40–0.90)], lower shoulder flexibility [0.54 (0.30–0.98)] and a higher aerobic capacity [0.61 (0.40–0.93)], and higher odds for NSP if they had greater abdominal endurance [1.57(1.07–2.31)] and greater bimanual dexterity [1.77(1.18–2.65)]. Females showed a U shaped relationship between NSP and back endurance [low: 2.12 (1.20–3.74); high 2.12 (1.18–3.83)].ConclusionAdolescent NSP was associated with fitness and motor competence, although the associations varied with gender, and their strength was limited.
MCP-1-deficient mice show reduced neuroinflammatory responses and increased peripheral inflammatory responses to peripheral endotoxin insult
Authors: Thompson Wendy L , Karpus William J , Van Eldik Linda J 
Published: August 2008

AbstractBackgroundAn endotoxin insult mimics a severe peripheral infection and recent evidence suggests that a single exposure can cause long-term cognitive deficits. A peripheral injection of LPS results in production of pro-inflammatory cytokines, such as IL-1β and TNF-α, in the brain and periphery and these cytokines mediate many effects of the acute phase response including activation of the HPA axis. The chemokine MCP-1 is highly expressed during endotoxemia and although much is known about the importance of MCP-1 in peripheral inflammatory responses to LPS, information about MCP-1 and CNS responses to peripheral LPS is lacking.MethodsC57Bl/6 mice were administered LPS by intraperitoneal (i.p.) injection, serum and brains were collected at several time points, and the time course of MCP-1 protein up-regulation was measured. To examine the role of MCP-1 in activation of the brain during acute systemic inflammation, we injected MCP-1 knockout (MCP-1-/-) or control C57Bl/6 (MCP-1+/+) mice with LPS i.p. and measured the levels of selected cytokines and chemokines in serum and brain extracts 6 hours later. Activated microglia were examined by CD45 immunohistochemistry, and serum corticosterone and ACTH levels were measured by enzyme immunoassay.ResultsWe report that LPS injection induces a robust increase in MCP-1 protein levels in serum and brain, with peak brain levels reached at 6 hrs after LPS administration. MCP-1-/-mice injected with LPS showed higher levels of serum IL-1β and TNF-α compared to LPS-treated MCP-1+/+mice. In contrast, these MCP-1-/-mice showed significantly lower inductions of brain pro-inflammatory cytokines and chemokines, fewer activated microglia, and a reduction in serum corticosterone levels.ConclusionMCP-1-/-mice have decreased brain inflammation after a peripheral LPS insult, despite an exaggerated peripheral response. These data demonstrate an important role for MCP-1 in regulation of brain inflammation after peripheral endotoxemia.
The Frizzled 3 gene is associated with methamphetamine psychosis in the Japanese population
Authors: Kishimoto Makiko , Ujike Hiroshi , Okahisa Yuko , Kotaka Tatsuya , Takaki Manabu , Kodama Masafumi , Inada Toshiya , Yamada Mitsuhiko , Uchimura Naohisa , Iwata Nakao , Sora Ichiro , Iyo Masaomi , Ozaki Norio , Kuroda Shigetoshi 
Published: August 2008

Abstract

Background
Frizzled 3 (Fzd3) is a receptor required for the Wnt-signaling pathway, which has been implicated in the development of the central nervous system, including synaptogenesis and structural plasticity. We previously found a significant association between the FZD3 gene and susceptibility to schizophrenia, but subsequent studies showed inconsistent findings. To understand the roles of the FZD3 gene in psychotic disorders further, it should be useful to examine FZD3 in patients with methamphetamine psychosis because the clinical features of methamphetamine psychosis are similar to those of schizophrenia.

Methods
Six SNPs of FZD3, rs3757888 in the 3' flanking region, rs960914 in the intron 3, rs2241802, a synonymous SNP in the exon5, rs2323019 and rs352203 in the intron 5, and rs880481 in the intron 7, were selected based on the previous schizophrenic studies and analyzed in 188 patients with methamphetamine psychosis and 240 age- and gender-matched controls.

Results
A case-control association analyses revealed that two kinds of FZD3 haplotypes showed strong associations with methamphetamine psychosis (p < 0.00001). Having the G-A-T-G or A-G-C-A haplotype of rs2241802-rs2323019-rs352203-rs880481 was a potent negative risk factor (odds ratios were 0.13 and 0.086, respectively) for methamphetamine psychosis.

Conclusion
Our present and previous findings indicate that genetic variants of the FZD3 gene affect susceptibility to two analogous but distinct dopamine-related psychoses, endogenous and substance-induced psychosis.
Capsular synovial metaplasia mimicking silicone leak of a breast prosthesis: a case report
Authors: Krishnanandan Sarah , Abbassian Ali , Sharma Anup K , Cunnick Giles 
Published: August 2008

Abstract

Introduction
Synovial metaplasia around a prosthesis and in particular around silicone breast implants has been noted by various investigators, but has unknown clinical significance. We report on a patient where a large amount of synovial fluid mimicked rupture of an implant. We believe this to be an unusual clinical presentation of this phenomenon. Review of the English language literature failed to identify a comparable case.

Case presentation
A 25-year-old woman had undergone bilateral breast augmentation for cosmetic reasons. One implant was subsequently subjected to two attempts at expansion to correct asymmetry. The patient was later found to have a large quantity of viscous fluid around the port of that same prosthesis. Histological assessment of the implant had consequently confirmed capsular synovial metaplasia. This had initially caused the suspicion of a silicone 'bleed' from the implant and had resulted in an unnecessary explantation.

Conclusion
Capsular synovial metaplasia should be ruled out before the removal of breast implants where a leak is suspected. Manipulation and expansion of an implant may be risk factors for the development of synovial metaplasia.
Interferon-induced protein IFIT4 is associated with systemic lupus erythematosus and promotes differentiation of monocytes into dendritic cell-like cells
Authors: Huang Xiangyang , Shen Nan , Bao Chunde , Gu Yueying , Wu Li , Chen Shunle 
Published: August 2008

Abstract
Introduction
Using oligonucleotide microarray, many IFN-inducible genes have been found to be highly expressed in peripheral blood mononuclear cells (PBMCs) from most patients with systemic lupus erythematosus (SLE). Among these IFN-inducible genes, IFN-induced protein with tetratricopeptide repeats 4 (IFIT4) is a novel gene whose function is unknown.

Methods
In this study we examined the role played by IFIT4 in monocyte differentiation and the correlation between IFIT4 expression and the clinical manifestation of SLE. To this end, we used plasmid transfection, flow cytometry, mixed leucocyte responses, ELISA, quantitative RT-PCR and Western blotting.

Results
We found that both IFIT4 mRNA and protein expression levels were significantly higher in PBMCs and monocytes from SLE patients than in those from healthy control individuals. IFIT4 expression was positively correlated with antinuclear antibodies, anti-double-stranded DNA, and anti-Sm auto-immune antibodies in SLE. Patients with SLE exhibiting higher expression of IFIT4 had a higher prevalence of leucopenia, thrombocytopenia and C3/C4 decrease. IFIT4 protein was localized exclusively to the cytoplasm, and it was significantly upregulated by IFN-α in normal PBMCs. To determine the role played by IFIT4 in monocyte differentiation, the monocytic cell line THP-1 was transfected with pEGFP-IFIT4 expression plasmid and stimulated with granulocyte-macrophage colony-stimulating factor/IL-4 to generate IFIT4-primed dendritic cell-like cells (DCLCs). IFIT4-primed DCLCs acquired morphological characteristics of dendritic cells more quickly, with greater resemblance to dendritic cells, as compared with DCLCs primed with pEGFP-C1 control plasmid trasfection. Furthermore, they exhibited higher expressions of CD40, CD86, CD80, HLA-DR and CD83, along with lower expression of CD14; increased IL-12 secretion; and an increased ability to stimulate T-cell proliferation. In addition, IFIT4-primed DCLCs enhanced IFN-γ secretion (about 2.4-fold) by T cells compared with controls.

Conclusion
Our findings suggest that IFIT4 might play roles in promoting monocyte differentiation into DCLCs and in directing DCLCs to modulate T-helper-1 cell differentiation; these actions might contribute to the autoimmunity and pathogenesis of SLE.
Recombinant human activated protein C attenuates endotoxin-induced lung injury in awake sheep
Authors: Waerhaug Kristine , Kuklin Vladimir N , Kirov Mikhail Y , Sovershaev Mikhail A , Langbakk Bodil , Ingebretsen Ole C , Ytrehus Kirsti , Bjertnaes Lars J 
Published: August 2008

Abstract
Introduction
Acute lung injury often complicates severe sepsis. In Gram-negative sepsis, bacterial endotoxin activates both coagulation and inflammation. Enhanced lung vascular pressures and permeability, increased extravascular lung water content and deteriorated gas exchange characterize ovine endotoxin-induced lung injury, a frequently used model of acute lung injury. Recombinant human activated protein C (rhAPC), with its anticoagulant, anti-inflammatory, fibrinolytic and antiapoptotic effects, reportedly reduces the respirator-dependent days and the mortality of patients with severe sepsis. We speculate whether rhAPC antagonizes endotoxin-induced lung injury in sheep.

Methods
Two groups of sheep were exposed to Escherichia coli endotoxin (lipopolysaccharide) 15 ng/kg/minute intravenously from 0 to 24 hours; one group received only lipopolysaccharide throughout (n = 8), and the other group received lipopolysaccharide in combination with rhAPC 24 μg/kg/hour from 4 to 24 hours (n = 9). In addition, one group received rhAPC as above as the only intervention (n = 4), and four sham-operated sheep were used for determination of the α and ε isoforms of protein kinase C in pulmonary tissue. Data were assessed by one-way analysis of variance for repeated measurements. Biochemical data were analyzed using Student's t test, or using the Mann–Whitney U test when appropriate.

Results
Infusion of endotoxin caused lung injury, manifested by increments in pulmonary artery pressure, in pulmonary micro-occlusion pressure, in pulmonary vascular downstream resistance, in pulmonary vascular permeability index, in extravascular lung water index and in deterioration of oxygenation that were all attenuated by infusion of rhAPC. Endotoxemia led to changes in inflammation and coagulation, including pulmonary neutrophil accumulation paralleled by increased TNFα and decreased protein C and fibrinogen in animal plasma, which all improved following infusion of rhAPC. Moreover, rhAPC prevented the translocation of protein kinase C α and ε isoforms from the cytosolic fraction of lung tissue extracts.

Conclusion
In awake sheep, rhAPC alleviates endotoxin-induced lung injury – as characterized by improvements of oxygenation, coagulation and inflammation, as well as by reversal of pulmonary hemodynamic and volumetric changes.
Time course of plasma gelsolin concentrations during severe sepsis in critically ill surgical patients
Authors: Wang HaiHong , Cheng BaoLi , Chen QiXing , Wu ShuiJing , Lv Chen , Xie GuoHao , Jin Yue , Fang XiangMing 
Published: August 2008

Abstract
Introduction
Gelsolin is an actin-binding plasma protein that is part of an 'actin-scavenging' system. Studies suggest that plasma gelsolin may play a crucial role in the pathophysiology of sepsis. Little is known about the course of plasma gelsolin levels over time in patients with severe sepsis. The aim of the study was to investigate plasma gelsolin levels in severe septic patients and to determine whether these levels predict the severity or clinical outcome of severe sepsis.

Methods
Ninety-one patients who were diagnosed with severe sepsis at admission to a surgical intensive care unit were enrolled, and admission plasma gelsolin levels were recorded. Plasma gelsolin levels were recorded daily in 23 of these patients. Daily plasma gelsolin levels were recorded in an additional 15 nonseptic critically ill patients. Fifteen volunteers served as healthy control individuals. Plasma gelsolin levels were measured using an enzyme-linked immunosorbent assay. Concentrations of IL-6, IL-10 and tumour necrosis factor (TNF)-α were also measured on intensive care unit admission.

Results
The admission gelsolin levels were significantly decreased in severe sepsis (20.6 ± 11.7 mg/l) compared with nonseptic critically ill patients (52.3 ± 20.3 mg/l; P < 0.001) and healthy control individuals (126.8 ± 32.0 mg/l; P < 0.001). Severe septic patients had increased IL-6 levels compared with nonseptic critically ill patients (20.0 ± 10.7 pg/ml versus 11.4 ± 13.9 pg/ml; P = 0.048), whereas no significant difference in IL-10 or TNF-α levels was observed (IL-10: 97.9 ± 181.5 pg/ml versus 47.4 ± 91.5 pg/ml, respectively [P = 0.425]; TNF-α: 14.2 ± 13.9 pg/ml versus 6.9 ± 5.3 pg/ml, respectively; P = 0.132). Survivors of severe sepsis exhibited substantial recovery of their depressed plasma gelsolin levels, whereas gelsolin levels in nonsurvivors remained at or below their depleted admission levels.

Conclusion
Plasma gelsolin may be a valuable marker for severe sepsis. Recovery of depleted plasma gelsolin levels correlated with clinical improvement. The prognostic role of plasma gelsolin in critical illness requires further investigation in a large cohort.
MotifCluster: an interactive online tool for clustering and visualizing sequences using shared motifs
Authors: Hamady Micah , Widmann Jeremy , Copley Shelley D , Knight Rob 
Published: August 2008

AbstractMotifCluster finds related motifs in a set of sequences, and clusters the sequences into families using the motifs they contain. MotifCluster, at http://bmf.colorado.edu/motifcluster, lets users test whether proteins are related, cluster sequences by shared conserved motifs, and visualize motifs mapped onto trees, sequences and three-dimensional structures. We demonstrate MotifCluster's accuracy using gold-standard protein superfamilies; using recommended settings, families were assigned to the correct superfamilies with 0.17% false positive and no false negative assignments.
Vitamin D3 induces pro-LL-37 expression in myeloid precursors from patients with severe congenital neutropenia
Authors: Karlsson Jenny , Carlsson Göran , Larne Olivia , Andersson Mats , Pütsep Katrin 
Published: August 2008

AbstractThe innate immune system produces a number of effector molecules that are important for protection against bacterial infections. Neutrophils and antimicrobial peptides are major components of innate defense with the capacity of rapid bacterial killing. Patients with severe congenital neutropenia (SCN) experience recurrent and chronic infections despite recombinant G-CSF-mobilized neutrophils. We have shown previously that these neutrophils are deficient in that they lack the antimicrobial peptide LL-37. Here, we show that pro-LL-37 mRNA is not expressed in neutrophil precursors from patients with SCN, although the gene and promoter region for pro-LL-37, CAMP, does not display any mutations. The hormonal form of vitamin D3 [1,25(OH)2D3] induced the expression of pro-LL-37 in isolated neutrophil progenitors and in EBV-transformed B cells from patients with SCN, whereas all-trans retinoic acid only induced expression in transformed B cells. These results demonstrate that myeloid cells of patients with SCN can produce pro-LL-37, suggesting that other pathways are impaired.