bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intraprostatic Botulinum Toxin Type A injection in patients with benign prostatic enlargement: duration of the effect of a single treatment
Authors: Silva João , Pinto Rui , Carvalho Tiago , Botelho Francisco , Silva Pedro , Oliveira Rui , Silva Carlos , Cruz Francisco , Dinis Paulo 
Published: August 2009

Abstract

Background
Botulinum Toxin Type-A (BoNT/A) intraprostatic injection can induce prostatic involution and improve LUTS and urinary flow in patients with Benign Prostatic Enlargement (BPE). However, the duration of these effects is unknown. The objective of this work was to determine the duration of prostate volume reduction after one single intraprostatic injection of 200U of Botulinum Toxin Type-A.

Methods
This is an extension of a 6 month study in which 21 frail elderly patients with refractory urinary retention and unfit for surgery were submitted to intraprostatic injection of BoNT/A-200U, by ultrasound guided transrectal approach. In spite of frail conditions, eleven patients could be followed during 18 months. Prostate volume, total serum PSA, maximal flow rate (Qmax), residual volume (PVR) and IPSS-QoL scores were determined at 1, 3, 6, 12 and 18 months post-treatment.

Results
Mean prostate volume at baseline, 82 ± 16 ml progressively decreased from month one coming to 49 ± 9,5 ml (p = 0,003) at month six. From this moment on, prostate volume slowly recovered, becoming identical to baseline at 18 months (73 ± 16 ml, p = 0.03). Albeit non significant, serum PSA showed a 25% decrease from baseline to month 6. The 11 patients resumed spontaneous voiding at month one. Mean Qmax was 11,3 ± 1,7 ml/sec and remained unchanged during the follow-up period. PVR ranged from 55 ± 17 to 82 ± 20 ml and IPSS score from10 to 12 points.

Conclusion
Intraprostatic BoNT/A injection is safe and can reduce prostate volume for a period of 18 months. During this time a marked symptomatic improvement can be maintained.
Changes in cultured endothelial cell glycosaminoglycans under hyperglycemic conditions and the effect of insulin and heparin
Authors: Han Juying , Zhang Fuming , Xie Jin , Linhardt Robert J , Hiebert Linda M 
Published: August 2009

Abstract

Background
Heparan sulfate proteoglycans (HSPGs) contain glycosaminoglycan (GAG) chains made primarily of heparan sulfate (HS). Hyperglycemia in diabetes leads to endothelial injury and nephropathy, retinopathy and atherosclerosis. Decreased HSPG may contribute to diabetic endothelial injury. Decreased tissue HS in diabetes has been reported, however, endothelial HS changes are poorly studied.

Objective
To determine total GAGs, including HS, in endothelium under hyperglycemic conditions and the protective effect of insulin and heparin.

Methods
Confluent primary porcine aortic endothelial cells (PAECs) were divided into control, glucose (30 mM), insulin (0.01 unit/ml) and glucose plus insulin treatment groups for 24, 48 and 72 hours. Additionally, PAECs were treated with glucose, heparin (0.5 μ g/ml) and glucose plus heparin for 72 hours. GAGs were isolated from cells and medium. GAG concentrations were determined by the carbazole assay and agarose gel electrophoresis.

Results
GAGs were significantly increased only in control and glucose plus insulin groups at 72 versus 24 hours. Glucose decreased cell GAGs and increased medium GAGs, and insulin alone decreased cell GAGs at all times compared to control. In the glucose plus insulin group, cell GAGs were less than control at 24 hours, and greater than glucose or insulin alone at 48 and 72 hours while GAGs in medium were greater than control at all times and glucose at 72 hours. Heparin increased GAGs in glucose treated cells and medium.

Conclusion
High glucose and insulin alone reduces endothelial GAGs. In hyperglycemic conditions, heparin or insulin preserves GAGs which may protect cells from injury. Insulin is an effective diabetic therapy since it not only lowers blood glucose, but also protects endothelium.
Respiratory and skin health among glass microfiber production workers: a cross-sectional study
Authors: Sripaiboonkij Penpatra , Sripaiboonkij Nintita , Phanprasit Wantanee , Jaakkola Maritta S 
Published: August 2009

Abstract

Background
Only a few studies have investigated non-malignant respiratory effects of glass microfibers and these have provided inconsistent results. Our objective was to assess the effects of exposure to glass microfibers on respiratory and skin symptoms, asthma and lung function.

Methods
A cross-sectional study of 102 workers from a microfiber factory (response rate 100%) and 76 office workers (73%) from four factories in Thailand was conducted. They answered a questionnaire on respiratory health, occupational exposures, and lifestyle factors, and performed spirometry. Measurements of respirable dust were available from 2004 and 2005.

Results
Workers exposed to glass microfibers experienced increased risk of cough (adjusted OR 2.04), wheezing (adjOR 2.20), breathlessness (adjOR 4.46), nasal (adjOR 2.13) and skin symptoms (adjOR 3.89) and ever asthma (adjOR 3.51), the risks of breathlessness (95%CI 1.68–11.86) and skin symptoms (1.70–8.90) remaining statistically significant after adjustment for confounders. There was an exposure-response relation between the risk of breathlessness and skin symptoms and increasing level of microfiber exposure. Workers exposed to sensitizing chemicals, including phenol-formaldehyde resin, experienced increased risk of cough (3.43, 1.20–9.87) and nasal symptoms (3.07, 1.05–9.00).

Conclusion
This study provides evidence that exposure to glass microfibers increases the risk of respiratory and skin symptoms, and has an exposure-response relation with breathlessness and skin symptoms. Exposure to sensitizing chemicals increased the risk of cough and nasal symptoms. The results suggest that occupational exposure to glass microfibers is related to non-malignant adverse health effects, and that implementing exposure control measures in these industries could protect the health of employees.
JNK1 activation predicts the prognostic outcome of the human hepatocellular carcinoma
Authors: Chang Qingshan , Chen Jianguo , Beezhold Kevin J , Castranova Vince , Shi Xianglin , Chen Fei 
Published: August 2009

Abstract

Background
Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide with an extremely poor prognosis. The classification of HCC based on the molecular signature is not well-established.

Results
In the present study, we reported HCC signature genes based on the JNK1 activation status in 31 HCC specimens relative to the matched distal noncancerous liver tissue from 31 patients. The HCCs with high JNK1 (H-JNK1) and low JNK1 (L-JNK1) were sub-grouped. Two different signature gene sets for both H-JNK1 and L-JNK1 HCC were identified through gene expression profiling. A striking overlap of signature genes was observed between the H-JNK1 HCC and the hepatoblastoma or hepatoblastoma-type HCC. Many established biomarkers for hepatic progenitor cells were over-expressed in H-JNK1 HCC, including AFP, TACSTD1, KRT19, KRT7, THY1, and PROM1. In addition, the majority of the most up-regulated genes were those associated with metastasis and earlier recurrence, whereas the genes for normal liver function were substantially down-regulated in H-JNK1 HCC tissue. A Kaplan-Meier plot demonstrated that the survival of the patients with H-JNK1 HCC was severely impaired.

Conclusion
Accordingly, we believe that the H-JNK1 HCC may originate from hepatic progenitor cells and is associated with poorer prognosis. The status of JNK1 activation in HCC tissue, thus, might be a new biomarker for HCC prognosis and therapeutic targeting.
Cardiac magnetic resonance versus transthoracic echocardiography for the assessment of cardiac volumes and regional function after myocardial infarction: an intrasubject comparison using simultaneous intrasubject recordings
Authors: Gardner Blake I , Bingham Scott E , Allen Marvin R , Blatter Duane D , Anderson Jeffrey L 
Published: August 2009

Abstract

Background
Although echocardiography is commonly used to evaluate cardiac function after MI, CMR may provide more accurate functional assessment but has not been adequately compared with echo. The primary study objective was to compare metrics of left ventricular volumes and global and regional function determined by cardiac magnetic resonance (CMR) and echocardiography (echo) in patients (pts) with recent myocardial infarction (MI).

Methods
To compare CMR with echo, 47 consecutive patients (pts 70% male; mean age = 66 ± 11 years) with MI >6 wks previously and scheduled for imaging evaluation were studied by both echo and CMR within 60 min of each other. Readers were blinded to pt information. Pearson's correlation coefficient, paired t-tests, and chi-square tests were used to compare CMR and echo measures. Further comparisons were made between pts and 30 normal controls for CMR and between pts and published normal ranges for echo.

Results
Measures of volume and function correlated moderately well between CMR and echo (r = 0.54 to 0.75, all p < 0.001), but large and systematic differences were noted in absolute measurements. Echo underestimated left ventricular (LV) volumes (by 69 ml for end-diastolic, 35 ml for end-systolic volume, both p < 0.001), stroke volume (by 34 ml, p < 0.001), and LV ejection fraction (LVEF) (by 4 percentage point, p = 0.02). CMR was much more sensitive to detection of segmental wall motion abnormalities (p < 0.001). CMR comparisons with normal controls confirmed an increase in LV volumes, a decrease in LVEF, and preservation of stroke volume after MI.

Conclusion
This intra subject comparison after MI found large, systematic differences between CMR and echo measures of volumes, LVEF, and wall motion abnormality despite moderate inter-modality correlations, with echo underestimating each metric. CMR also provided superior detection and quantification of segmental function after MI. Serial studies of LV function in individual patients should use the same modality.
The Drosophila immunoglobulin gene turtle encodes guidance molecules involved in axon pathfinding
Authors: Al-Anzi Bader , Wyman Robert J 
Published: August 2009

Abstract
Background
Neuronal growth cones follow specific pathways over long distances in order to reach their appropriate targets. Research over the past 15 years has yielded a large body of information concerning the molecules that regulate this process. Some of these molecules, such as the evolutionarily conserved netrin and slit proteins, are expressed in the embryonic midline, an area of extreme importance for early axon pathfinding decisions. A general model has emerged in which netrin attracts commissural axons towards the midline while slit forces them out. However, a large number of commissural axons successfully cross the midline even in the complete absence of netrin signaling, indicating the presence of a yet unidentified midline attractant.

Results
The evolutionarily conserved Ig proteins encoded by the turtle/Dasm1 genes are found in Drosophila, Caenorhabditis elegans, and mammals. In Drosophila the turtle gene encodes five proteins, two of which are diffusible, that are expressed in many areas, including the vicinity of the midline. Using both molecular null alleles and transgenic expression of the different isoforms, we show that the turtle encoded proteins function as non-cell autonomous axonal attractants that promote midline crossing via a netrin-independent mechanism. turtle mutants also have either stalled or missing axon projections, while overexpression of the different turtle isoforms produces invasive neurons and branching axons that do not respect the histological divisions of the nervous system.

Conclusion
Our findings indicate that the turtle proteins function as axon guidance cues that promote midline attraction, axon branching, and axonal invasiveness. The latter two capabilities are required by migrating axons to explore densely packed targets.
The influence of human papillomavirus type and HIV status on the lymphomononuclear cell profile in patients with cervical intraepithelial lesions of different severity
Authors: Gonçalves Maria Alice G , Soares Edson G , Donadi Eduardo A 
Published: August 2009

AbstractBackgroundImmunological alterations are implicated in the increased prevalence of high-grade squamous intraepithelial lesions (HG-SIL) and persistent human papillomavirus (HPV) infection. This study evaluated the expression of CD4, CD8, CD25 (IL-2Rα) and CD28 antigens from SIL biopsies, stratified by HIV status and HPV-type. Biopsies specimens from 82 (35 HIV+) women with a normal cervix, low-grade (LG-SIL) or high-grade lesions (HG-SIL) were studied. CD molecule expression was evaluated by immunohistochemistry and HPV detection/typing performed using PCR techniques.ResultsCD4 stromal staining was increased in patients with HPV18. Women with HPV16 infection showed decreased: a) CD8 and CD25 stromal staining, b) CD25 staining in LG-SIL epithelium and in HG-SIL stroma. In HIV-women samples, CD28 epithelial staining and CD8 stromal staining surrounding metaplastic epithelium were less intense and even absent, as compared to HIV+women. Both epithelial and stromal CD8 staining was more intense in the HG-SIL/HIV+group than in the HG-SIL/HIV-group. Positive correlations were observed between CD4/CD25, CD4/CD28 and CD25/CD28 in the stroma and CD25/CD28 in the epithelium.ConclusionHIV status and HPV-type may influence the lymphomononuclear cell profile present in the spectrum of cervical lesions. The knowledge of the infiltrating cell profile in cervical tumours may help the development of specific anti-tumoural strategies.
Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ
Authors: Kelchtermans Hilde , Schurgers Evelien , Geboes Lies , Mitera Tania , Van Damme Jo , Van Snick Jacques , Uyttenhove Catherine , Matthys Patrick 
Published: August 2009

Abstract
Introduction
Interleukin (IL)-17 is a pro-inflammatory cytokine in rheumatoid arthritis (RA) and collagen-induced arthritis (CIA). Since interferon (IFN)-γ inhibits Th17 cell development, IFN-γ receptor knockout (IFN-γR KO) mice develop CIA more readily. We took advantage of this model to analyse the mechanisms of action of IL-17 in arthritis. The role of IFN-γ on the effector mechanisms of IL-17 in an in vitro system was also investigated.

Methods
IFN-γR KO mice induced for CIA were treated with anti-IL-17 or control antibody. The collagen type II (CII)-specific humoral and cellular autoimmune responses, myelopoiesis, osteoclastogenesis, and systemic cytokine production were determined. Mouse embryo fibroblasts (MEF) were stimulated with IL-17, tumor necrosis factor (TNF)-α and the expression of cytokines and chemokines were determined.

Results
A preventive anti-IL-17 antibody treatment inhibited CIA in IFNγR KO mice. In the joints of anti-IL-17-treated mice, neutrophil influx and bone destruction were absent. Treatment reduced the cellular autoimmune response as well as the splenic expansion of CD11b+ cells, and production of myelopoietic cytokines such as granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-6. IL-17 and TNF-α synergistically induced granulocyte chemotactic protein-2 (GCP-2), IL-6 and receptor activator of NFκB ligand (RANKL) in MEF. This induction was profoundly inhibited by IFN-γ in a STAT-1 (signal transducer and activator of transcription-1)-dependent way.

Conclusions
In the absence of IFN-γ, IL-17 mediates its pro-inflammatory effects mainly through stimulatory effects on granulopoiesis, neutrophil infiltration and bone destruction. In vitro IFN-γ profoundly inhibits the effector function of IL-17. Thus, aside from the well-known inhibition of the development of Th17 cells by IFN-γ, this may be an additional mechanism through which IFN-γ attenuates autoimmune diseases.
Development and validation of the self-administered Fibromyalgia Assessment Status: a disease-specific composite measure for evaluating treatment effect
Authors: Salaffi Fausto , Sarzi-Puttini Piercarlo , Girolimetti Rita , Gasparini Stefania , Atzeni Fabiola , Grassi Walter 
Published: August 2009

Abstract
Introduction
The Fibromyalgia Impact Questionnaire (FIQ) is a composite disease-specific measure validated for fibromyalgia (FM), but it is rarely used in clinical practice. The objective was to develop and analyse the psychometric properties of a new composite disease-specific index (Fibromyalgia Assessment Status, FAS), a simple self-administered index that combines a patient's assessment of fatigue, sleep disturbances and pain evaluated on the basis of the 16 non-articular sites listed on the Self-Assessment Pain Scale (SAPS) in a single measure (range 0 to 10).

Methods
The FAS index was constructed using a traditional development strategy, and its psychometric properties were tested in 226 FM patients (209 women, 17 men); whose disease-related characteristics were assessed by means of an 11-numbered circular numerical rating scale (NRS) for pain, fatigue, sleep disturbances and general health (GH), the tender point score (TPS), the SAPS, the FIQ, and the SF-36. A group of 226 rheumatoid arthritis (RA) patients was used for comparative purposes. Of the 179 FM patients who entered the follow-up study, 152 completed the three-month period and were included in the responsiveness analyses. One hundred and fifty-four patients repeated the FAS questionnaire after an interval of one week, and its test/re-test reliability was calculated. Responsiveness was evaluated on the basis of effect size and the standardised response mean.

Results
The FAS index fulfilled the established criteria for validity, reliability and responsiveness. Factor analysis showed that SAPS and fatigue contributed most, and respectively explained 47.4% and 31.2% of the variance; sleep explained 21.3%. Testing for internal consistency showed that Cronbach's alpha was 0.781, thus indicating a high level of reliability. As expected, closer significant correlations were found when FAS was compared with total FIQ (rho = 0.347; P < 0.0001) and the FIQ subscales, particularly job ability, tiredness, fatigue and pain (all P < 0.0001), but the correlation between FAS and the mental component summary scale score (MCS) of the SF-36 (rho = -0.531; P < 0.0001) was particularly interesting. Test/re-test reliability was satisfactory. The FAS showed the greatest effect size. The magnitude of the responsiveness measures was statistically different between FAS (0.889) and the FIQ (0.781) (P = 0.038), and between the SF-36 MCS (0.434) and the SF-36 physical component summary scale score (PCS) (0.321) (P < 0.01).

Conclusions
The self-administered FAS is a reliable, valid and responsive disease-specific composite measure for assessing treatment effect in patients with FM.
CCR1-mediated activation of nuclear factor-κB in THP-1 monocytic cells involvespertussistoxin-insensitive Gα14 and Gα16 signaling cascades
Authors: Lee Maggie M K , Wong Yung H 
Published: August 2009

AbstractMultiple signaling intermediates are involved in the regulation of nuclear factor-kB by chemokines in monocytic cells.Agonists of CC chemokine receptor CCR1 contribute to the pathogenesis of autoimmune and other inflammatory diseases, possibly via the regulation of the transcription factor NF-κB. CCR1 and CCR2b have been demonstrated to use PTX-insensitive Gα14 and Gα16 to stimulate PLCβ in cotransfected cells, and Gα14 and Gα16 are capable of activating NF-κB. The coexpression of Gα14, Gα16, and CCR1 in human monocytic THP-1 cells suggests that CCR1 may use Gα14 or Gα16 to induce NF-κB activation. Here, we demonstrated that a CCR1 agonist, Lkn-1, stimulated NF-κB phosphorylation via PTX-insensitive G proteins in THP-1 cells. Lkn-1 also mediated IKK/NF-κB phosphorylations in HEK293 cells overexpressing CCR1 and Gα14/16. Using various kinase inhibitors, Raf-1, MEK1/2, PLCβ, PKC, CaM, CaMKII, and c-Src were found to participate in Lkn-1-stimulated IKK/NF-κB phosphorylations in THP-1 and transfected HEK293 cells. Although c-Jun N-terminal kinase and p38 MAPK were activated by Lkn-1, they were not required in Lkn-1-induced IKK phosphorylation. The ability of CCR1 to signal through Gα14/16 thus provides a linkage for chemokines to regulate NF-κB-dependent responses.
Dre recombinase, like Cre, is a highly efficient site-specific recombinase in E. coli, mammalian cells and mice
Authors: Anastassiadis Konstantinos , Fu Jun , Patsch Christoph , Hu Shengbiao , Weidlich Stefanie , Duerschke Kristin , Buchholz Frank , Edenhofer Frank , Stewart A. Francis 
Published: August 2009

SUMMARY
Tyrosine site-specific recombinases (SSRs) including Cre and FLP are essential tools for DNA and genome engineering. Cre has long been recognized as the best SSR for genome engineering, particularly in mice. Obtaining another SSR that is as good as Cre will be a valuable addition to the genomic toolbox. To this end, we have developed and validated reagents for the Dre-rox system. These include an Escherichia coli-inducible expression vector based on the temperature-sensitive pSC101 plasmid, a mammalian expression vector based on the CAGGs promoter, a rox-lacZ reporter embryonic stem (ES) cell line based on targeting at the Rosa26 locus, the accompanying Rosa26-rox reporter mouse line, and a CAGGs-Dre deleter mouse line. We also show that a Dre-progesterone receptor shows good ligand-responsive induction properties. Furthermore, we show that there is no crossover recombination between Cre-rox or Dre-loxP. Hence, we add another set of efficient tools to the genomic toolbox, which will enable the development of more sophisticated mouse models for the analysis of gene function and disease.
The Analysis of Masts and Towers
Authors: Nielsen Mogens G. 
Published: August 2009

For many years both guyed masts and self-supporting towers have been used for supporting antennas for mobile and other communications. The choice between masts and towers has often been determined by the tradition. However masts have its clear advantages in the open country, whereas the towers are more likely to be chosen in the urban areas. Masts and towers are often used for broadcasting of radio and television or antennas for cellular phones. The masts and towers consequently are situated on the top of hills and mountains, where the climate often is extreme with respect to wind load and in some cases due to atmospheric icing. Since the wind is turbulent and the masts and towers are flexible and sensitive to dynamic load, the dynamic response becomes important in the analysis of towers and guyed masts. However there are some differences in the analysis of masts and towers. The wind resistance for lattice sections is dependent on the type of members, the solidity of the sections and for tubular members also dependant on the Reynolds number. Furthermore, latest research within the IASS Working Group for Masts and Towers has shown that the wind resistance of tubular sections is dependent on the turbulence of the wind. The masts act strongly in non-linear fashion since the guy ropes are varying from slackened to a taut string. Over the years different methods have been used for analysing guyed masts making the methods more and more realistic: starting by a gust factor method, over the IASS patch wind method to the Eurocode patch wind method, which gives results close to the results from a stochastic analysis and the time domain analysis. The towers do not act as non-linear as the masts. However, the towers are also sensitive to the dynamics of the wind and a dynamic factor should be applied depending on the turbulence of the wind, the height of the structure etc.