bluuebunny/crossref_metadata_2025_split huggingface dataset:
Type-2 diabetes-induced changes in vascular extracellular matrix gene expression: Relation to vessel size
Authors: Song WeiWei , Ergul Adviye 
Published: February 2006

Abstract

Background
Hyperglycemia-induced changes in vascular wall structure contribute to the pathogenesis of diabetic microvascular and macrovascular complications. Matrix metalloproteinases (MMP), a family of proteolytic enzymes that degrade extracellular matrix (ECM) proteins, are essential for vascular remodeling. We have shown that endothelin-1 (ET-1) mediates increased MMP activity and associated vascular remodeling in Type 2 diabetes. However, the effect of Type 2 diabetes and/or ET-1 on the regulation of ECM and MMP gene expression in different vascular beds remains unknown.

Methods
Aorta and mesenteric artery samples were isolated from control, Type 2 diabetic Goto-Kakizaki (GK) rats and GK rats treated with ETA antagonist ABT-627. Gene expression profile of MMP-2, MMP-9, MT1-MMP, fibronectin, procollagen type 1, c-fos and c-jun, were determined by quantitative real-time (qRT) PCR. In addition, aortic gene expression profile was evaluated by an ECM & Adhesion Molecules pathway specific microarray approach.

Results
Analysis of the qRT-PCR data demonstrated a significant increase in mRNA levels of MMPs and ECM proteins as compared to control animals after 6 weeks of mild diabetes. Futhermore, these changes were comparable in aorta and mesentery samples. In contrast, treatment with ETA antagonist prevented diabetes-induced changes in expression of MMPs and procollagen type 1 in mesenteric arteries but not in aorta. Microaarray analysis provided evidence that 27 extracellular matrix genes were differentially regulated in diabetes. Further qRT-PCR with selected 7 genes confirmed the microarray data.

Conclusion
These results suggest that the expression of both matrix scaffold protein and matrix degrading MMP genes are altered in macro and microvascular beds in Type 2 diabetes. ETA antagonism restores the changes in gene expression in the mesenteric bed but not in aorta suggesting that ET-1 differentially regulates microvascular gene expression in Type 2 diabetes.
Therapeutic efficacy test in malaria falciparum in Antioquia, Colombia
Authors: Blair Silvia , Carmona-Fonseca Jaime , Piñeros Juan G , Ríos Alexandra , Álvarez Tania , Álvarez Gonzalo , Tobón Alberto 
Published: February 2006

AbstractObjectiveEvaluate the frequency of failure of eight treatments for non-complicated malaria caused byPlasmodium falciparumin patients from Turbo (Urabá region), El Bagre and Zaragoza (Bajo Cauca region), applying the 1998 protocol of the World Health Organization (WHO). Monotherapies using chloroquine (CQ), amodiaquine (AQ), mefloquine (MQ) and sulphadoxine-pyrimethamine (SP), and combinations using chloroquine-sulphadoxine-pyrimethamine (CQ-SP), amodiaquine-sulphadoxine-pyrimethamine (AQ-SP), mefloquine-sulphadoxine-pyrimethamine (MQ-SP) and artesunate-sulphadoxine-pyrimethamine (AS-SP), were examined.MethodologyA balanced experimental design with eight groups. Samples were selected based on statistical and epidemiological criteria. Patients were followed for 21 to 28 days, including seven or eight parasitological and clinical evaluations, with an active search for defaulting patients. A non-blinded evaluation of the antimalarial treatment response (early failure, late failure, adequate response) was performed.ResultsInitially, the loss of patients to follow-up was higher than 40%, but the immediate active search for the cases and the monetary help for transportation expenses of patients, reduced the loss to 6%. The treatment failure was: CQ 82%, AQ 30%, MQ 4%, SP 24%, CQ-SP 17%, AQ-SP 2%, MQ-S-P 0%, AS-SP 3%.ConclusionThe characteristics of an optimal epidemiological monitoring system of antimalarial treatment response in Colombia are discussed. It is proposed to focus this on early failure detection, by applying a screening test every two to three years, based on a seven to 14-day follow-up. Clinical and parasitological assessment would be carried out by a general physician and a field microscopist from the local hospital, with active measures to search for defaulter patients at follow-up.
Are insecticide-treated bednets more protective against Plasmodium falciparum than Plasmodium vivax- infected mosquitoes?
Authors: Bockarie Moses J , Dagoro Henry 
Published: February 2006

Abstract

Background
The outcomes of insecticide-treated bednet (ITN) interventions for malaria control in Papua New Guinea tend to suggest a differential protective effect against Plasmodium falciparum and Plasmodium vivax. Little is known about the impact of ITNs on the relative abundance of mosquitoes infected with either P. falciparum or P. vivax. This paper describes the biting cycle of P. falciparum and P. vivax-infected mosquitoes and the impact of an ITN intervention on the proportion of mosquitoes infected with either parasite species.

Methods
Entomological investigations were performed in East Sepik (ESP) and New Ireland Provinces (NIP) of PNG. Mosquitoes were collected using the all-night (18:00 - 06:00) landing catch and CDC light-trap methods and species specific malaria sporozoite rates were determined by ELISA.

Results and discussion
The distribution of sporozoite positive mosquitoes in three four-hour periods (18:00-22:00, 22:00-02:00 & 02:00-06:00) showed that a higher proportion of P. vivax-infected mosquitoes were biting before people retired to bed under the protection of bednets. In the intervention village, the 308 mosquitoes collected before ITNs were introduced included eight (2.0%) P. falciparum-positive and four (1.0%) P. vivax- positive specimens, giving a parasite ratio of 2:1. The sporozoite rate determined from 908 mosquitoes caught after ITNs were introduced showed a significant decrease for P. falciparum (0.7%) and a slight increase for P. vivax (1.3%), resulting in a post intervention parasite ratio of 1:2. In the East Sepik Province, where ITNs were not used, P. falciparum remained the dominant species in 12 monthly mosquito collections and monthly P. falciparum:P. vivax formula varied from 8:1 to 1.2:1.

Conclusion
These findings suggest that people sleeping under treated bednets may be more exposed to P. vivax than P. falciparum-infected mosquitoes before going to sleep under the protection of bednets. This difference in the biting behaviour of mosquitoes infected with different malaria parasites may partly explain the change in the P. falciparum:P. vivax formula after the introduction of ITNs.
IL-4 alpha chain receptor (IL-4Rα) polymorphisms in allergic bronchopulmonary sspergillosis
Authors: Knutsen Alan P , Kariuki Barbara , Consolino Judy D , Warrier Manoj R 
Published: February 2006

AbstractBackgroundAllergic bronchopulmonary aspergillosis occurs in 7–10% of cystic fibrosis (CF) and 1–2% of asthmatic patients. HLA-DR restriction and increased sensitivity to IL-4 stimulation have been proposed as risk factors in these populations.ObjectiveWe examined for the presence of IL-4 receptor alpha chain (IL-4Rα) single nucleotide polymorphisms (SNPs) in ABPA and whether these accounted for increased sensitivity to IL-4 stimulation.MethodsOne extracellular (ile75val) and four cytoplasmic IL-4Rα SNPs were analyzed in 40 CF and 22 asthmatic patients and in 56 non-ABPA CF and asthmatic patients. Sensitivity to IL-4 stimulation was measured by induction of CD23 expression on B cells.ResultsIL-4Rα SNPs were observed in 95% of ABPA patients. The predominant IL-4Rα SNP was the extracellular IL-4Rα SNP, ile75val, observed in 80% of ABPA patients.ConclusionThe presence of IL-4Rα SNPs, principally ile75val, appears to be a genetic risk for the development of ABPA.
Macrophage metalloelastase (MMP-12) deficiency does not alter bleomycin-induced pulmonary fibrosis in mice
Authors: Manoury Boris , Nenan Soazig , Guenon Isabelle , Boichot Elisabeth , Planquois Jean-Michel , Bertrand Claude P , Lagente Vincent 
Published: February 2006

Abstract

Background
Pulmonary fibrosis is characterized by excessive deposition of extracellular matrix in the interstitium resulting in respiratory failure. The role of remodeling mediators such as metalloproteinases (MMPs) and their inhibitors (TIMPs) in the fibrogenic process remains misunderstood. In particular, macrophage metalloelastase, also identified as MMP-12, is known to be involved in remodeling processes under pathological conditions. However, MMP-12 involvement in pulmonary fibrosis is unknown. Here we investigated fibrotic response to bleomycin in MMP-12 deficient mice.

Materials and methods
C57BL/6 mice, Balb/c mice and MMP-12 -/- mice with a C57BL/6 background received 0.3 mg bleomycin by intranasal administration. 14 days after, mice were anesthetized and underwent either bronchoalveolear lavage (BAL) or lung removal. Collagen deposition in lung tissue was determined by Sircol™ collagen assay, MMP activity in BAL fluid was analyzed by zymography, and other mediators were quantified in BAL fluid by ELISA. Real time PCR was performed to assess gene expression in lung removed one or 14 days after bleomycin administration. Student t test or Mann & Whitney tests were used when appropriate for statistical analysis.

Results
The development of pulmonary fibrosis in "fibrosis prone" (C57BL/6) mice was associated with prominent MMP-12 expression in lung, whereas MMP-12 expression was weak in lung tissue of "fibrosis resistant" (Balb/c) mice. MMP-12 mRNA was not detected in MMP-12 -/- mice, in conformity with their genotype. Bleomycin elicited macrophage accumulation in BAL of MMP-12 -/- and wild type (WT) mice, and MMP-12 deficiency had no significant effect on BAL cells composition. Collagen content of lung was increased similarly in MMP-12 -/- and WT mice 14 days after bleomycin administration. Bleomycin elicit a raise of TGF-β protein, MMP-2 and TIMP-1 protein and mRNA in BAL fluids and lung respectively, and no significant difference was observed between MMP-12 -/- and WT mice considering those parameters.

Conclusion
The present study shows that MMP-12 deficiency has no significant effect on bleomycin-induced fibrosis.
Predictors of job satisfaction among doctors, nurses and auxiliaries in Norwegian hospitals: relevance for micro unit culture
Authors: Krogstad Unni , Hofoss Dag , Veenstra Marijke , Hjortdahl Per 
Published: February 2006

Abstract

Objective
To explore what domains of work are important for job satisfaction among doctors, nurses and auxiliaries and to discuss differences between professional groups in the perspective of micro team culture.

Design
Cross-sectional survey data from hospital staff working clinically at inpatient hospital wards in Norway in 2000.

Measures
Linear regression models predicting job satisfaction for the three professions were compared. First, five domains of hospital work were examined for general job satisfaction. Based on the result of the first regression, five items concerning local leadership were explored in a second regression.

Results
A total of 1814 doctors, nurses and auxiliaries working at 11 Norwegian hospitals responded (overall response rate: 65%). The only domain of work that significantly predicted high job satisfaction important for all groups was positive evaluation of local leadership. Both steps of analyses suggested that professional development is most important for doctors. For registered nurses, experiencing support and feedback from the nearest superior was the main explanatory variable for job satisfaction. Job satisfaction of auxiliaries was equally predicted by professional development and local leadership. The results are discussed and interpreted as reflections of cultural values, loyalties and motivation.

Conclusion
The professional values of medicine, the organizational and holistic skills of nurses and the practical experience of auxiliaries should all be valued in the building of interdependent micro teams.
Distinguishing between linear and exponential cell growth during the division cycle: Single-cell studies, cell-culture studies, and the object of cell-cycle research
Authors: Cooper Stephen 
Published: February 2006

Abstract

Background
Two approaches to understanding growth during the cell cycle are single-cell studies, where growth during the cell cycle of a single cell is measured, and cell-culture studies, where growth during the cell cycle of a large number of cells as an aggregate is analyzed. Mitchison has proposed that single-cell studies, because they show variations in cell growth patterns, are more suitable for understanding cell growth during the cell cycle, and should be preferred over culture studies. Specifically, Mitchison argues that one can glean the cellular growth pattern by microscopically observing single cells during the division cycle. In contrast to Mitchison's viewpoint, it is argued here that the biological laws underlying cell growth are not to be found in single-cell studies. The cellular growth law can and should be understood by studying cells as an aggregate.

Results
The purpose or objective of cell cycle analysis is presented and discussed. These ideas are applied to the controversy between proponents of linear growth as a possible growth pattern during the cell cycle and the proponents of exponential growth during the cell cycle. Differential (pulse) and integral (single cell) experiments are compared with regard to cell cycle analysis and it is concluded that pulse-labeling approaches are preferred over microscopic examination of cell growth for distinguishing between linear and exponential growth patterns. Even more to the point, aggregate experiments are to be preferred to single-cell studies.

Conclusion
The logical consistency of exponential growth – integrating and accounting for biochemistry, cell biology, and rigorous experimental analysis – leads to the conclusion that proposals of linear growth are the result of experimental perturbations and measurement limitations. It is proposed that the universal pattern of cell growth during the cell cycle is exponential.
Glutathione and growth inhibition of Mycobacterium tuberculosis in healthy and HIV infected subjects
Authors: Venketaraman Vishwanath , Rodgers Tatanisha , Linares Rafael , Reilly Nancy , Swaminathan Shobha , Hom David , Millman Ariel C , Wallis Robert , Connell Nancy D 
Published: February 2006

AbstractIntracellular levels of glutathione are depleted in patients with acquired immunodeficiency syndrome in whom the risk of tuberculosis, particularly disseminated disease is many times that of healthy individuals. In this study, we examined the role of glutathione in immunity against tuberculosis infection in samples derived from healthy and human immunodeficiency virus infected subjects. Our studies confirm that glutathione levels are reduced in peripheral blood mononuclear cells and in red blood cells isolated from human immunodeficiency virus-infected subjects (CD4>400/cumm). Furthermore, treatment of blood cultures from human immunodeficiency virus infected subjects with N-acetyl cysteine, a glutathione precursor, caused improved control of intracellularM. tuberculosisinfection. N-acetyl cysteine treatment decreased the levels of IL-1, TNF-α, and IL-6, and increased the levels of IFN-γ in blood cultures derived from human immunodeficiency virus-infected subjects, promoting the host immune responses to containM. tuberculosisinfection successfully.
Cytokine expression in mice exposed to diesel exhaust particles by inhalation. Role of tumor necrosis factor
Authors: Saber Anne T , Jacobsen Nicklas R , Bornholdt Jette , Kjær Sanna L , Dybdahl Marianne , Risom Lotte , Loft Steffen , Vogel Ulla , Wallin Håkan 
Published: February 2006

AbstractBackgroundParticulate air pollution has been associated with lung and cardiovascular disease, for which lung inflammation may be a driving mechanism. The pro-inflammatory cytokine, tumor necrosis factor (TNF) has been suggested to have a key-role in particle-induced inflammation.We studied the time course of gene expression of inflammatory markers in the lungs of wild type mice andTnf-/-mice after exposure to diesel exhaust particles (DEPs). Mice were exposed to either a single or multiple doses of DEP by inhalation. We measured the mRNA level of the cytokinesTnfand interleukin-6(Il-6)and the chemokines, monocyte chemoattractant protein(Mcp-1), macrophage inflammatory protein-2(Mip-2)and keratinocyte derived chemokine(Kc)in the lung tissue at different time points after exposure.ResultsTnfmRNA expression levels increased late after DEP-inhalation, whereas the expression levels ofIl-6,Mcp-1andKcincreased early. The expression ofMip-2was independent of TNF if the dose was above a certain level. The expression levels of the cytokinesKc,Mcp-1andIl-6, were increased in the absence of TNF.ConclusionOur data demonstrate thatTnfis not important in early DEP induced inflammation and rather exerts negative influence onMcp-1andKcmRNA levels. This suggests that other signalling pathways are important, a candidate being one involvingMcp-1.
Quantitative analysis of the epithelial lining architecture in radicular cysts and odontogenic keratocysts
Authors: Landini Gabriel 
Published: February 2006

Abstract

Background
This paper describes a quantitative analysis of the cyst lining architecture in radicular cysts (of inflammatory aetiology) and odontogenic keratocysts (thought to be developmental or neoplastic) including its 2 counterparts: solitary and associated with the Basal Cell Naevus Syndrome (BCNS).

Methods
Epithelial linings from 150 images (from 9 radicular cysts, 13 solitary keratocysts and 8 BCNS keratocysts) were segmented into theoretical cells using a semi-automated partition based on the intensity of the haematoxylin stain which defined exclusive areas relative to each detected nucleus. Various morphometrical parameters were extracted from these "cells" and epithelial layer membership was computed using a systematic clustering routine.

Results
Statistically significant differences were observed across the 3 cyst types both at the morphological and architectural levels of the lining. Case-wise discrimination between radicular cysts and keratocyst was highly accurate (with an error of just 3.3%). However, the odontogenic keratocyst subtypes could not be reliably separated into the original classes, achieving discrimination rates slightly above random allocations (60%).

Conclusion
The methodology presented is able to provide new measures of epithelial architecture and may help to characterise and compare tissue spatial organisation as well as provide useful procedures for automating certain aspects of histopathological diagnosis.
Methotrexate in rheumatoid arthritis is frequently effective, even if re-employed after a previous failure
Authors: Kapral Theresa , Stamm Tanja , Machold Klaus P , Montag Karin , Smolen Josef S , Aletaha Daniel 
Published: February 2006

AbstractEffectiveness of therapy with individual disease-modifying antirheumatic drugs (DMARDs) in rheumatoid arthritis (RA) is limited, and the number of available DMARDs is finite. Therefore, at some stage during the lengthy course of RA, institution of traditional DMARDs that have previously been applied may have to be reconsidered. In the present study we investigated the effectiveness of re-employed methotrexate in patients with a history of previous methotrexate failure (original course). A total of 1,490 RA patients (80% female, 59% rheumatoid factor positive) were followed from their first presentation, yielding a total of 6,470 patient-years of observation. We identified patients in whom methotrexate was re-employed after at least one intermittent course of a different DMARD. We compared reasons for discontinuation, improvement in acute phase reactants, and cumulative retention rates of methotrexate therapy between the original course of methotrexate and its re-employment. Similar analyses were peformed for other DMARDs. Methotrexate was re-employed in 86 patients. Compared with the original courses, re-employment was associated with a reduced risk for treatment termination because of ineffectiveness (P= 0.02, by McNemar test), especially if the maximum methotrexate dose of the original course had been low (<12.5 mg/week;P= 0.02, by logistic regression). In a Cox regression model, re-employed MTX was associated with a significantly reduced hazard of treatment termination compared with the original course of methotrexate, adjusting for dose and year of employment (hazard ratio 0.64, 95% confidence interval 0.42–0.97;P= 0.04). These findings were not recapitulated in analyses of re-employment of other DMARDs. Re-employment of MTX despite prior inefficacy, but not re-employment of other DMARDs, is an effective therapeutic option, especially in those patients in whom the methotrexate dose of the original course was low.
Vitamin D receptor gene BsmIpolymorphisms in Thai patients with systemic lupus erythematosus
Authors: Sakulpipatsin Wilaiporn , Verasertniyom Oravan , Nantiruj Kanokrat , Totemchokchyakarn Kitti , Lertsrisatit Porntawee , Janwityanujit Suchela 
Published: February 2006

AbstractThe immunomodulatory role of 1,25-dihydroxyvitamin D3 is well known. An association between vitamin D receptor (VDR) gene BsmI polymorphisms and systemic lupus erythematosus (SLE) has been reported. To examine the characteristics of VDR gene BsmI polymorphisms in patients with SLE and the relationship of polymorphisms to the susceptibility and clinical manifestations of SLE, VDR genotypings of 101 Thai patients with SLE and 194 healthy controls were performed based on polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The relationship between VDR gene BsmI polymorphisms and clinical manifestations of SLE was evaluated. The distribution of VDR genotyping in patients with SLE was 1.9% for BB (non-excisable allele homozygote), 21.78% for Bb (heterozygote), and 76.23% for bb (excisable allele homozygote). The distribution of VDR genotyping in the control group was 1.03% for BB, 15.98% for Bb, and 82.99% for bb. There was no statistically significant difference between the two groups (p = 0.357). The allelic distribution of B and b was similar within the groups (p = 0.173). The relationship between VDR genotype and clinical manifestation or laboratory profiles of SLE also cannot be statistically demonstrated. In conclusion, we cannot verify any association between VDR gene BsmI polymorphism and SLE. A larger study examining other VDR gene polymorphisms is proposed.