bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stromal upregulation of lateral epithelial adhesions: Gene expression analysis of signalling pathways in prostate epithelium
Authors: Chambers Karen F , Pearson Joanna F , Pellacani Davide , Aziz Naveed , Gužvić Miodrag , Klein Christoph A , Lang Shona H 
Published: June 2011

Abstract

Background
Stromal signalling increases the lateral cell adhesions of prostate epithelial cells grown in 3D culture. The aim of this study was to use microarray analysis to identify significant epithelial signalling pathways and genes in this process.

Methods
Microarray analysis was used to identify genes that were differentially expressed when epithelial cells were grown in 3D Matrigel culture with stromal co-culture compared to without stroma. Two culture models were employed: primary epithelial cells (ten samples) and an epithelial cell line (three experiments). A separate microarray analysis was performed on each model system and then compared to identify tissue-relevant genes in a cell line model.

Results
TGF beta signalling was significantly ranked for both model systems and in both models the TGF beta signalling gene SOX4 was significantly down regulated. Analysis of all differentially expressed genes to identify genes that were common to both models found several morphology related gene clusters; actin binding (DIAPH2, FHOD3, ABLIM1, TMOD4, MYH10), GTPase activator activity (BCR, MYH10), cytoskeleton (MAP2, MYH10, TMOD4, FHOD3), protein binding (ITGA6, CD44), proteinaceous extracellular matrix (NID2, CILP2), ion channel/ ion transporter activity (CACNA1C, CACNB2, KCNH2, SLC8A1, SLC39A9) and genes associated with developmental pathways (POFUT1, FZD2, HOXA5, IRX2, FGF11, SOX4, SMARCC1).

Conclusions
In 3D prostate cultures, stromal cells increase lateral epithelial cell adhesions. We show that this morphological effect is associated with gene expression changes to TGF beta signalling, cytoskeleton and anion activity.
Physiologic and molecular consequences of endothelial Bmpr2 mutation
Authors: Majka Susan , Hagen Moira , Blackwell Thomas , Harral Julie , Johnson Jennifer A , Gendron Robert , Paradis Helene , Crona Daniel , Loyd James E , Nozik-Grayck Eva , Stenmark Kurt R , West James 
Published: June 2011

AbstractBackgroundPulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations. However, the physiologic and molecular consequences of expression of BMPR2 mutations in PMVEC are unknown.MethodsIn vivo experiments were performed on adult mice with conditional endothelial-specific expression of the truncation mutation Bmpr2delx4+, with age-matched transactivator-only mice as controls. Phenotype was assessed by RVSP, counts of muscularized vessels and proliferating cells, and staining for thromboses, inflammatory cells, and apoptotic cells. The effects of BMPR2 knockdown in PMVEC by siRNA on rates of apoptosis were assessed. Affymetrix expression arrays were performed on PMVEC isolated and cultured from triple transgenic mice carrying the immortomouse gene, a transactivator, and either control, Bmpr2delx4+or Bmpr2R899Xmutation.ResultsTransgenic mice showed increased RVSP and corresponding muscularization of small vessels, with histologic alterations including thrombosis, increased inflammatory cells, increased proliferating cells, and a moderate increase in apoptotic cells. Expression arrays showed alterations in specific pathways consistent with the histologic changes. Bmpr2delx4+and Bmpr2R899Xmutations resulted in very similar alterations in proliferation, apoptosis, metabolism, and adhesion; Bmpr2delx4+cells showed upregulation of platelet adhesion genes and cytokines not seen in Bmpr2R899XPMVEC. Bmpr2 mutation in PMVEC does not cause a loss of differentiation markers as was seen with Bmpr2 mutation in smooth muscle cells.ConclusionsBmpr2 mutation in PMVECin vivomay drive PAH through multiple, potentially independent, downstream mechanisms, including proliferation, apoptosis, inflammation, and thrombosis.
Pneumonia and poverty: a prospective population-based study among children in Brazil
Authors: Thörn Lícia KAM , Minamisava Ruth , Nouer Simonne S , Ribeiro Luiza H , Andrade Ana Lucia 
Published: June 2011

Abstract

Background
Children in developing country suffer the highest burden of pneumonia. However, few studies have evaluated associations between poverty and pneumonia.

Methods
A prospective population-based study on pneumonia was carried out as part of the Latin America Epidemiological Assessment of Pneumococcus (LEAP study). Chest x-rays were obtained for children one to 35 months old with suspected pneumonia presenting to emergency care centers and hospital emergency rooms in Goiania, Brazil. Chest radiographs were evaluated according to WHO guidelines. Clustering of radiologically-confirmed pneumonia were evaluated using a Poisson-based spatial scan statistic. Associations between census socioeconomic indicators and pneumonia incidence rates were analyzed using generalized linear models.

Results
From May, 2007 to May, 2009, chest radiographs were obtained from 11 521 children with clinical pneumonia; 3955 episodes were classified as radiologically-confirmed. Incidence rates were significantly higher in very low income areas (4825.2 per 105) compared to high income areas (1637.3 per 105). Spatial analysis identified clustering of confirmed pneumonia in Western (RR 1.78; p = 0.001) and Southeast (RR 1.46; p = 0.001) regions of the city, and clustering of hospitalized pneumonia in the Western region (RR 1.69; p = 0.001). Lower income households and illiteracy were associated with pneumonia incidence.

Conclusions
In infants the risk of developing pneumonia is inversely associated with the head of household income and with the woman educational level. Areas with deprived socioeconomic conditions had higher incidence of pneumonia and should be targeted for high vaccination coverage.
Alternative health care consultations in Ontario, Canada: A geographic and socio-demographic analysis
Authors: Williams Allison M , Kitchen Peter , Eby Jeanette 
Published: June 2011

Abstract

Background
An important but understudied component of Canada's health system is alternative care. The objective of this paper is to examine the geographic and socio-demographic characteristics of alternative care consultation in Ontario, Canada's largest province.

Methods
Data is drawn from the Canadian Community Health Survey (CCHS Cycle 3.1, 2005) for people aged 18 or over (n = 32,598) who had a consultation with an alternative health care provider. Four groups of consultations are examined: (1) all consultations (2) massage therapy (3) acupuncture, and (4) homeopath/naturopath. Descriptive statistics, mapping and logistic regression modeling are employed to analyze the data and to compare modalities of alternative health care use.

Results
In 2005, more than 1.2 million adults aged 18 or over consulted an alternative health care provider, representing about 13% of the total population of Ontario. The analysis revealed a varied geographic pattern of consultations across the province. Consultations were fairly even across the urban to rural continuum and rural residents were just as likely to consult a provider as their urban counterparts. From a health perspective, people with a chronic condition, lower health status and self-perceived unmet health care needs were more likely to see an alternative health provider. Women with chronic conditions such as fibromyalgia, high blood pressure, chronic fatigue syndrome and chemical sensitivities were more likely to see an alternative provider if they felt their health care needs were not being met.

Conclusions
The analysis revealed that geography is not a factor in determining alternative health care consultations in Ontario. By contrast, there is a strong association between these consultations and socio-demographic characteristics particularly age, sex, education, health and self-perceived unmet health care needs. The results underscore the importance of women's health needs as related to alternative care use. The paper concludes that there is a need for more place-specific research that explores the reasons why people use specific types of alternative health care as tied to socio-economic status, health, place of residence, and knowledge of these treatments.
Increased serum myeloid-related protein 8/14 level is associated with atherosclerosis in type 2 diabetic patients
Authors: Peng Wen Hui , Jian Wei Xia , Li Hai Ling , Hou Lei , Wei Yi Dong , Li Wei Ming , Xu Ya Wei 
Published: June 2011

Abstract

Background
Myeloid-related protein 8/14 (MRP8/14) is a stable heterodimer formed by two different calcium-binding proteins (MRP8 and MRP14). Studies have identified that MRP8/14 regulates vascular inflammation and serves as a novel marker of acute coronary syndrome. In this study, we evaluated the correlation between serum levels of MRP8/14, hsCRP, endogenous secretory receptor for advanced glycation end-products (esRAGE) and the occurrence of coronary artery disease (CAD), or carotid intima-media thickness (IMT) when CAD was not yet developed in diabetic patients.

Methods
Serum levels of MRP8/14, esRAGE and hsCRP were measured in 375 diabetic patients. Then the results of those who had CAD were compared against who had not. Also, we investigated the associations between above-mentioned indicators and IMT of subjects without CAD in both diabetic group and non-diabetic one.

Results
Serum MRP8/14 was significantly higher in CAD than in non-CAD group (9.7 ± 3.6 ug/ml vs. 8.2 ± 3.0 ug/ml, P < 0.001). It was associated with severity of CAD (r = 0.16, P = 0.026). In non-CAD group, MRP8/14 was associated with IMT in patients with (r = 0.30, P < 0.001) or without diabetes (r = 0.26, P = 0.015). The areas under the curves of receiver operating characteristic for CAD were 0.63 (95% CI 0.57-0.68) for MRP8/14, 0.76 (95% CI 0.71-0.81) for hsCRP and 0.62 (95% CI 0.56 -0.67) for esRAGE.

Conclusion
In summary, we report that diabetic patients with CAD had elevated plasma MRP8/14 levels which were also positively correlated with the severity of CAD and carotid IMT in patients without clinically overt CAD.
Temporal trends in serum concentrations of polychlorinated dioxins, furans, and PCBs among adult women living in Chapaevsk, Russia: a longitudinal study from 2000 to 2009
Authors: Humblet Olivier , Sergeyev Oleg , Altshul Larisa , Korrick Susan A , Williams Paige L , Emond Claude , Birnbaum Linda S , Burns Jane S , Lee Mary M , Revich Boris , Shelepchikov Andrey , Feshin Denis , Hauser Russ 
Published: June 2011

Abstract

Background
The present study assessed the temporal trend in serum concentrations of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls (PCBs) among residents of a Russian town where levels of these chemicals are elevated due to prior industrial activity.

Methods
Two serum samples were collected from eight adult women (in 2000 and 2009), and analyzed with gas chromatography-high-resolution mass spectrometry.

Results
The average total toxic equivalency (TEQ) decreased by 30% (from 36 to 25 pg/g lipid), and the average sum of PCB congeners decreased by 19% (from 291 to 211 ng/g lipid). Total TEQs decreased for seven of the eight women, and the sum of PCBs decreased for six of eight women. During this nine year period, larger decreases in serum TEQs and PCBs were found in women with greater increases in body mass index.

Conclusions
This study provides suggestive evidence that average serum concentrations of dioxins, furans, and PCBs are decreasing over time among residents of this town.
Developmental regulation of the neuroinflammatory responses to LPS and/or hypoxia-ischemia between preterm and term neonates: An experimental study
Authors: Brochu Marie-Elsa , Girard Sylvie , Lavoie Karine , Sébire Guillaume 
Published: June 2011

Abstract

Background
Preterm and term newborns are at high risk of brain damage as well as subsequent cerebral palsy and learning disabilities. Indeed, hypoxia-ischemia (HI), pathogen exposures, and associated intracerebral increase of pro-inflammatory cytokines have all been linked to perinatal brain damage. However, the developmental effects of potential variations of pro- and anti-inflammatory cytokine ratios remain unknown.

Methods
Using rat models of perinatal brain damage induced by exposures to lipopolysaccharide (LPS) and/or HI at distinct levels of maturity, we compared cytokine expression at stages of cerebral development equivalent to either preterm (postnatal day 1, P1) or term (P12) newborns.

Results
At P1, expression of anti-inflammatory cytokine within the brain was either not modulated (IL-6, IL-10) or down-regulated (IL-1ra, TGF-β1) by HI, LPS or LPS+HI. In contrast, there was at P12 an up-regulation of all anti-inflammatory cytokines studied in HI or LPS+HI condition, but not after LPS exposure. Interestingly, IL-1β was the main pro-inflammatory cytokine up-regulated moderately at P1, and strongly at P12, with a weak co-expression of TNF-α observed mainly at P12. These age-dependant inflammatory reactions were also accompanied, under HI and LPS+HI conditions, at P12 only, by combined: (i) expression of chemokines CINC-1 and MCP-1, (ii) blood-brain barrier (BBB) leakage, and (iii) intracerebral recruitment of systemic immune cells such as neutrophils. In contrast, sole LPS induced IL-1β responses mainly within white matter at P1 and mainly within gray matter at P12, that were only associated with early MCP-1 (but no CINC-1) induction at both ages, without any recruitment of neutrophils and CD68+ cells.

Conclusion
HI and LPS+HI induce pro-inflammatory oriented immune responses in both preterm and term like brains, with a maximal inflammatory response triggered by the combination of LPS+HI. The profile of these neuroinflammatory responses presented striking variations according to age: no or down-regulated anti-inflammatory responses associated with mainly IL-1β release in preterm-like brains (P1), in sharp contrast to term-like brains (P12) presenting stronger anti-and pro-inflammatory responses, including both IL-1β and TNF-α releases, and BBB leakage. These developmental-dependant variations of neuroinflammatory response could contribute to the differential pattern of brain lesions observed across gestational ages in humans. This also highlights the necessity to take into consideration the maturation stage, of both brain and immune systems, in order to develop new anti-inflammatory neuroprotective strategies.
Array-based techniques for fingerprinting medicinal herbs
Authors: Niu Linhai , Mantri Nitin , Li Chun Guang , Xue Charlie , Pang Edwin 
Published: June 2011

Abstract
Poor quality control of medicinal herbs has led to instances of toxicity, poisoning and even deaths. The fundamental step in quality control of herbal medicine is accurate identification of herbs. Array-based techniques have recently been adapted to authenticate or identify herbal plants. This article reviews the current array-based techniques, eg oligonucleotides microarrays, gene-based probe microarrays, Suppression Subtractive Hybridization (SSH)-based arrays, Diversity Array Technology (DArT) and Subtracted Diversity Array (SDA). We further compare these techniques according to important parameters such as markers, polymorphism rates, restriction enzymes and sample type. The applicability of the array-based methods for fingerprinting depends on the availability of genomics and genetics of the species to be fingerprinted. For the species with few genome sequence information but high polymorphism rates, SDA techniques are particularly recommended because they require less labour and lower material cost.
Bovine spongiform encephalopathy infection alters endogenous retrovirus expression in distinct brain regions of cynomolgus macaques (Macaca fascicularis)
Authors: Greenwood Alex D , Vincendeau Michelle , Schmädicke Ann-Christin , Montag Judith , Seifarth Wolfgang , Motzkus Dirk 
Published: June 2011

Abstract

Background
Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease.

Results
Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques.

Conclusions
We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration.
Proteomic patterns of cervical cancer cell lines, a network perspective
Authors: Higareda-Almaraz Juan Carlos , Enríquez-Gasca María delRocío , Hernández-Ortiz Magdalena , Resendis-Antonio Osbaldo , Encarnación-Guevara Sergio 
Published: June 2011

AbstractBackgroundCervical cancer is a major mortality factor in the female population. This neoplastic is an excellent model for studying the mechanisms involved in cancer maintenance, because the Human Papilloma Virus (HPV) is the etiology factor in most cases. With the purpose of characterizing the effects of malignant transformation in cellular activity, proteomic studies constitute a reliable way to monitor the biological alterations induced by this disease. In this contextual scheme, a systemic description that enables the identification of the common events between cell lines of different origins, is required to distinguish the essence of carcinogenesis.ResultsWith this study, we sought to achieve a systemic perspective of the common proteomic profile of six cervical cancer cell lines, both positive and negative for HPV, and which differ from the profile corresponding to the non-tumourgenic cell line, HaCaT. Our objectives were to identify common cellular events participating in cancer maintenance, as well as the establishment of a pipeline to work with proteomic-derived results. We analyzed by means of 2D SDS-PAGE and MALDI-TOF mass spectrometry the protein extracts of six cervical cancer cell lines, from which we identified a consensus of 66 proteins. We call this group of proteins, the "central core of cervical cancer". Starting from this core set of proteins, we acquired a PPI network that pointed, through topological analysis, to some proteins that may well be playing a central role in the neoplastic process, such as 14-3-3ζ.In silicooverrepresentation analysis of transcription factors pointed to the overexpression of c-Myc, Max and E2F1 as key transcription factors involved in orchestrating the neoplastic phenotype.ConclusionsOur findings show that there is a "central core of cervical cancer" protein expression pattern, and suggest that 14-3-3ζ is key to determine if the cell proliferates or dies. In addition, our bioinformatics analysis suggests that the neoplastic phenotype is governed by a non-canonical regulatory pathway.
Discrete derivative: a data slicing algorithm for exploration of sharing biological networks between rheumatoid arthritis and coronary heart disease
Authors: Zheng Guang , Jiang Miao , He Xiaojuan , Zhao Jing , Guo Hongtao , Chen Gao , Zha Qinglin , Lu Aiping 
Published: June 2011

AbstractBackgroundOne important concept in traditional Chinese medicine (TCM) is "treating different diseases with the same therapy". In TCM practice, some patients with Rheumatoid Arthritis (RA) and some other patients with Coronary Heart Disease (CHD) can be treated with similar therapies. This suggests that there might be something commonly existed between RA and CHD, for example, biological networks or biological basis. As the amount of biomedical data in leading databases (i.e., PubMed, SinoMed, etc.) is growing at an exponential rate, it might be possible to get something interesting and meaningful through the techniques developed in data mining.ResultsBased on the large data sets of Western medicine literature (PubMed) and traditional Chinese medicine literature (SinoMed), by applying data slicing algorithm in text mining, we retrieved some simple and meaningful networks. The Chinese herbs used in treatment of both RA and CHD, might affect the commonly existed networks between RA and CHD. This might support the TCM concept of treating different diseases with the same therapy.ConclusionsFirst, the data mining results might show the positive answer that there are biological basis/networks commonly existed in both RA and CHD. Second, there are basic Chinese herbs used in the treatment of both RA and CHD. Third, these commonly existed networks might be affected by the basic Chinese herbs. Forth, discrete derivative, the data slicing algorithm is feasible in mining out useful data from literature of PubMed and SinoMed.
Correlation between endothelial function and carotid atherosclerosis in rheumatoid arthritis patients with long-standing disease
Authors: González-Juanatey Carlos , Llorca Javier , González-Gay Miguel A 
Published: June 2011

Abstract
Introduction
In this study, we aimed to determine the relationship between flow-mediated endothelium-dependent vasodilatation (FMD) and carotid artery intima-media wall thickness (IMT), two surrogate markers of atherosclerosis, in a series of Spanish patients with rheumatoid arthritis (RA) without clinically evident cardiovascular (CV) disease.

Methods
One hundred eighteen patients who fulfilled the 1987 American College of Rheumatology classification criteria for RA, had no history of CV disease and had at least one year of follow-up after disease diagnosis were randomly selected. Brachial and carotid ultrasonography were performed to determine FMD and carotid IMT, respectively.

Results
Carotid IMT values were higher and FMD percentages derived by performing ultrasonography were lower in individuals with a long duration from the time of disease diagnosis. Patients with a disease duration ≤ 7 years had significantly lower carotid IMT (mean ± SD) 0.69 ± 0.17 mm than those with long disease duration (0.81 ± 0.12 mm in patients with ≥ 20 years of follow-up). Also, patients with a long disease duration had severe endothelial dysfunction (FMD 4.0 ± 4.0% in patients with disease duration from 14.5 to 19.7 years) compared with those with shorter disease duration (FMD 7.4 ± 3.8% in patients with disease duration ≤ 7 years). Linear regression analysis revealed that carotid IMT was unrelated to FMD in the whole sample of 118 patients. However, carotid IMT was negatively associated with FMD when the time from disease diagnosis ranged from 7.5 to 19.7 years (P = 0.02).

Conclusions
In patients with RA without CV disease, endothelial dysfunction and carotid IMT increased with the duration of RA. The association between FMD and carotid IMT values was observed only in patients with long disease duration.