bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of monocyte chemotactic protein-3 and -4 in children with virus exacerbation of asthma
Authors: Santiago J. , Hernández-Cruz J. L. , Manjarrez-Zavala M. E. , Montes-Vizuet R. , Rosete-Olvera D. P. , Tapia-Díaz A. M. , Zepeda-Peney H. , Terán L. M. 
Published: June 2008

Macrophages play a crucial role in respiratory viral infections. However, the mechanisms by which these cells are recruited locally are not fully understood. The current authors studied the role of the chemokines monocyte chemotactic protein (MCP)-1, -2, -3 and -4 on monocyte/macrophage recruitment during respiratory viral infections. Levels of these chemokines were investigated in nasal aspirates from 6–12-yr-old children suffering from respiratory viral infections, caused by rhinoviruses, influenza viruses, parainfluenza viruses, adenoviruses and respiratory syncytial virus.MCP-3 and -4 were significantly higher in samples derived from virus-infected children compared with samples from the same children when they had been asymptomatic. Concentrations of both chemokines were found to significantly correlate with the number of recruited nasal macrophages. Chemotaxis assays showed that purified MCP-3 and -4 from nasal aspirates showed biological activityin vitro. There were no significant differences in MCP-1 and -2 levels between both groups.The present data indicates that monocyte chemotactic protein-3 and -4 may have an important role in macrophage recruitment in children with proven upper respiratory viral infections. These chemokines could be potential targets for therapeutic intervention in respiratory viral infections.
An epidemic of silicosis among former denim sandblasters
Authors: Akgun M. , Araz O. , Akkurt I. , Eroglu A. , Alper F. , Saglam L. , Mirici A. , Gorguner M. , Nemery B. 
Published: June 2008

Sandblasting denim using silica has emerged as a new cause of silicosis in Turkey. Following the discovery of several cases of silicosis in (young) workers who used this process, the frequency and main occupational risk factors of silicosis among former denim sandblasters in the region of Erzurum (Turkey) were evaluated.Demographic characteristics and information on working conditions were obtained by questionnaire and interview. In addition, spirometry testing was performed and chest radiographs were evaluated according to International Labour Office (ILO) classification of pneumoconioses in 157 former denim sandblasters.All subjects were male, with a mean (range) age of 23 (15–44) yrs. They had worked for a mean (range) of 36 (1–120) months, starting employment at a 17 (10–38) yrs of age. Most subjects (83%) had respiratory symptoms, especially dyspnoea (52%) but also chest pain (46%). Radiological evidence of silicosis (ILO score 1/0 or higher) was present in 77 (53%) out of 145 subjects with interpretable chest radiographs. These subjects had lower forced expiratory volume in one second and forced vital capacity. The risk of silicosis correlated with seniority (i.e.working as a foreman), exposure duration and number of places of work.Considering the high prevalence rate of silicosis in such workplaces, further problems are inevitable in the future unless effective measures are taken.
Clinical and polygraphic evolution of sleep-related breathing disorders in adolescents
Authors: Sánchez-Armengol A. , Ruiz-García A. , Carmona-Bernal C. , Botebol-Benhamou G. , García-Díaz E. , Polo-Padillo J. , López-Campos J. L. , Capote F. 
Published: June 2008

It has been suggested that sleep-related breathing disorders (SRBD) involve a continuum that develops over the course of life. If modifiable factors could be identified, the progression of SRBD could perhaps be addressed early in life. Although some studies have looked at the evolution of SRBD in pre-pubertal children, very few studies obtained data in adolescents.Anthropometric, clinical and polygraphic variables were collected during a 4-yr follow-up study among 148 normal adolescents after initial cross-sectional analysis.From a total of 267 adolescents studied at baseline (mean±sdage 14.3±2.1 yrs), 148 (55.4%) were followed up for 4 yrs. During follow-up, there were no significant changes in snoring and polygraphic parameters. However, a tendency toward weight gain with centrally distributed fat was observed. Habitual snorers had a significantly higher body mass index and more centrally distributed fat than nonsnorers. Males had a higher snoring prevalence and a higher number of respiratory events than females. Snoring at baseline, male sex and poor academic performance were significant predictors of snoring at follow-up.Snoring tends to persist during adolescence and male sex acts as a risk factor. A relationship between snoring and academic performance was observed. These findings may have implications for long-term management of sleep-related breathing disorders.
The modified BODE index: validation with mortality in COPD
Authors: Cote C. G. , Pinto-Plata V. M. , Marin J. M. , Nekach H. , Dordelly L. J. , Celli B. R. 
Published: June 2008

Peak oxygen uptake (V′O2) remains the gold standard measurement of exercise capacity and has been associated with survival. A modified BODE (body mass index, airflow obstruction, dyspnoea, exercise capacity) index replacing the 6-min walk distance (6MWD) withV′O2as % predicted (mBODE%) has been developed and found to have excellent correlation with the conventional BODE index.The objectives of the present study were to compare the ability of the conventional BODE and the mBODE% to predict mortality in 444 patients with chronic obstructive pulmonary disease (COPD) followed for a mean±sdperiod of 71±34 months. Anthropometrics, spirometry, lung volumes, comorbidity, cardiopulmonary cyclo-ergometry test and 6MWD were determined at entry.The mean BODE indices for the cohort were: BODE 4.1±2 and mBODE% 5.5±2. Both indices were significantly correlated with mortality. Logistic regression analysis with COPD survival as the dependent variable identified the BODE index, Charlson's and exercise capacity (in W) as variables associated with this outcome.In conclusion, the conventional BODE index, which uses the 6-min walk distance, predicts mortality in chronic obstructive pulmonary disease as well as the modified index using peak oxygen uptake. The results support the use of the simpler index, which includes the 6-min walk distance in the comprehensive evaluation of patients with chronic obstructive pulmonary disease.
Relationship between metabolic and genomic diversity in sesame (Sesamum indicum L.)
Authors: Laurentin Hernán , Ratzinger Astrid , Karlovsky Petr 
Published: June 2008

Abstract

Background
Diversity estimates in cultivated plants provide a rationale for conservation strategies and support the selection of starting material for breeding programs. Diversity measures applied to crops usually have been limited to the assessment of genome polymorphism at the DNA level. Occasionally, selected morphological features are recorded and the content of key chemical constituents determined, but unbiased and comprehensive chemical phenotypes have not been included systematically in diversity surveys. Our objective in this study was to assess metabolic diversity in sesame by nontargeted metabolic profiling and elucidate the relationship between metabolic and genome diversity in this crop.

Results
Ten sesame accessions were selected that represent most of the genome diversity of sesame grown in India, Western Asia, Sudan and Venezuela based on previous AFLP studies. Ethanolic seed extracts were separated by HPLC, metabolites were ionized by positive and negative electrospray and ions were detected with an ion trap mass spectrometer in full-scan mode for m/z from 50 to 1000. Genome diversity was determined by Amplified Fragment Length Polymorphism (AFLP) using eight primer pair combinations. The relationship between biodiversity at the genome and at the metabolome levels was assessed by correlation analysis and multivariate statistics.

Conclusion
Patterns of diversity at the genomic and metabolic levels differed, indicating that selection played a significant role in the evolution of metabolic diversity in sesame. This result implies that when used for the selection of genotypes in breeding and conservation, diversity assessment based on neutral DNA markers should be complemented with metabolic profiles. We hypothesize that this applies to all crops with a long history of domestication that possess commercially relevant traits affected by chemical phenotypes.
Molecular cloning and expression analysis of the STAT1 gene from olive flounder, Paralichthys olivaceus
Authors: Park Eun-Mi , Kang Jung-Ha , Seo Jung Soo , Kim GunDo , Chung Jongkyeong , Choi Tae-Jin 
Published: June 2008

Abstract

Background
Signal transducer and activator of transcription 1 (STAT1) is a critical component of interferon (IFN)-alpha/beta and IFN-gamma signaling. Although seven isoforms of STAT proteins have been reported from mammals, limited information is available for the STAT genes in fish. We isolated complementary DNA with high similarity to mammalian STAT1 from the olive flounder, Paralichthys olivaceus.

Results
A DNA fragment containing the conserved SH2 domain was amplified by RT-PCR using degenerate primers designed based on the highly conserved sequences in the SH2 domains of the zebrafish and mammalian STAT1. The complete cDNA sequence was obtained by 5' and 3' RACE. The flounder STAT1 transcript consisted of 2,909 bp that encoded a polypeptide of 749 amino acids. The overall similarity between flounder STAT1 and other STATs was very high, with the highest amino acid sequence identity to snakehead (89%). Phylogenetic analyses reveal that flounder STAT1 is in the same monophyletic group with snakehead STAT1. Quantitative real time RT-PCR and in situ hybridization revealed that STAT1 was expressed in almost all examined organs and tissues, with high expression in gill, spleen, kidney, and heart. The accumulation of STAT1 mRNA in different developmental stages, as determined by real time RT-PCR, increased with development.

Conclusion
Recent cloning of various cytokine genes and the STAT1 gene of olive flounder here suggest that fish also use the highly specialized JAK-STAT pathway for cytokine signaling. Identification of other STAT genes will elucidate in detail the signal transduction system in this fish.
Multiplex cytokine profile from dengue patients: MIP-1beta and IFN-gamma as predictive factors for severity
Authors: Bozza Fernando A , Cruz Oswaldo G , Zagne Sonia MO , Azeredo Elzinandes L , Nogueira Rita MR , Assis Edson F , Bozza Patricia T , Kubelka Claire F 
Published: June 2008

AbstractBackgroundDengue virus pathogenesis is not yet fully understood and the identification of patients at high risk for developing severe disease forms is still a great challenge in dengue patient care. During the present study, we evaluated prospectively the potential of cytokines present in plasma from patients with dengue in stratifying disease severity.MethodsSeventeen-cytokine multiplex fluorescent microbead immunoassay was used for the simultaneous detection in 59 dengue patients. GLM models using bimodal or Gaussian family were determined in order to associate cytokines with clinical manifestations and laboratory diagnosis.ResultsIL-1β, IFN-γ, IL-4, IL-6, IL-13, IL-7 and GM-CSF were significantly increased in patients with severe clinical manifestations (severe dengue) when compared to mild disease forms (mild dengue). In contrast, increased MIP-1β levels were observed in patients with mild dengue. MIP-1β was also associated with CD56+NK cell circulating rates. IL-1β, IL-8, TNF-α and MCP-1 were associated with marked thrombocytopenia. Increased MCP-1 and GM-CSF levels correlated with hypotension. Moreover, MIP-1β and IFN-γ were independently associated with both dengue severity and disease outcome.ConclusionOur data demonstrated that the use of a multiple cytokine assay platform was suitable for identifying distinct cytokine profiles associated with the dengue clinical manifestations and severity. MIP-β is indicated for the first time as a good prognostic marker in contrast to IFN-γ that was associated with disease severity.
Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injury
Authors: Nguyen Hal X , Galvan Manuel D , Anderson Aileen J 
Published: June 2008

AbstractBackgroundThe complement system has been suggested to affect injury or disease of the central nervous system (CNS) by regulating numerous physiological events and pathways. The activation of complement following traumatic CNS injury can also result in the formation and deposition of C5b-9 membrane attack complex (C5b-9/MAC), causing cell lysis or sublytic effects on vital CNS cells. Although complement proteins derived from serum/blood-brain barrier breakdown can contribute to injury or disease, infiltrating immune cells may represent an important local source of complement after injury. As the first immune cells to infiltrate the CNS within hours post-injury, polymorphonuclear leukocytes (PMNs) may affect injury through mechanisms associated with complement-mediated events. However, the expression/association of both early and terminal complement proteins by PMNs has not been fully characterized in vitro, and has not observed previously in vivo after traumatic spinal cord injury (SCI).MethodWe investigated the expression of complement mRNAs using rt-PCR and the presence of complement proteins associated with PMNs using immunofluroescence and quantitative flow cytometry.ResultsStimulated or unstimulated PMNs expressed mRNAs encoding for C1q, C3, and C4, but not C5, C6, C7 or C9 in culture. Complement protein C1q or C3 was also detected in less than 30% of cultured PMNs. In contrast, over 70% of PMNs that infiltrated the injured spinal cord were associated with C1q, C3, C7 and C5b-9/MAC 3 days post-SCI. The localization/association of C7 or C5b-9/MAC with infiltrating PMNs in the injured spinal cord suggests the incorporation or internalization of C7 or C5b-9/MAC bound cellular debris by infiltrating PMNs because C7 and C5b-9/MAC were mostly localized to granular vesicles within PMNs at the spinal cord epicenter region. Furthermore, PMN presence in the injured spinal cord was observed for many weeks post-SCI, suggesting that this infiltrating cell population could chronically affect complement-mediated events and SCI pathogenesis after trauma.ConclusionData presented here provide the first characterization of early and terminal complement proteins associated with PMNs in vitro and in vivo after SCI. Data also suggest a role for PMNs in the local internalization or deliverance of complement and complement activation in the post-SCI environment.
The effects of protein interactions, gene essentiality and regulatory regions on expression variation
Authors: Zhou Linqi , Ma Xiaotu , Sun Fengzhu 
Published: June 2008

Abstract

Background
Identifying factors affecting gene expression variation is a challenging problem in genetics. Previous studies have shown that the presence of TATA box, the number of cis-regulatory elements, gene essentiality, and protein interactions significantly affect gene expression variation. Nonetheless, the need to obtain a more complete understanding of such factors and how their interactions influence gene expression variation remains a challenge. The growth rates of yeast cells under several DNA-damaging conditions have been studied and a gene's toxicity degree is defined as the number of such conditions that the growth rate of the yeast deletion strain is significantly affected. Since toxicity degree reflects a gene's importance to cell survival under DNA-damaging conditions, we expect that it is negatively associated with gene expression variation. Mutations in both cis-regulatory elements and transcription factors (TF) regulating a gene affect the gene's expression and thus we study the relationship between gene expression variation and the number of TFs regulating a gene. Most importantly we study how these factors interact with each other influencing gene expression variation.

Results
Using yeast as a model system, we evaluated the effects of four separate factors and their interactions on gene expression variation: protein interaction degree, toxicity degree, number of TFs, and the presence of TATA box. Results showed that 1) gene expression variation is negatively correlated with the protein interaction degree in the protein interaction network, 2) essential genes tend to have less expression variation than non-essential genes and gene expression variation decreases with toxicity degree, and 3) the number of TFs regulating a gene is the most important factor influencing gene expression variation (R2 = 8–14%). In addition, the number of TFs regulating a gene was found to be an important factor influencing gene expression variation for both TATA-containing and non-TATA-containing genes, but with different association strength. Moreover, gene expression variation was significantly negatively correlated with toxicity degree only for TATA-containing genes.

Conclusion
The finding that distinct mechanisms may influence gene expression variation in TATA-containing and non-TATA-containing genes, provides new insights into the mechanisms that underlie the evolution of gene expression.
Induction of arthritis by high mobility group box chromosomal protein 1 is independent of tumour necrosis factor signalling
Authors: Pullerits Rille , Jonsson Ing-Marie , Kollias George , Tarkowski Andrej 
Published: June 2008

Abstract
Introduction
TNFα and high mobility group box chromosomal protein 1 (HMGB1) are two potent proinflammatory cytokines implicated as important mediators of arthritis. Increased levels of these cytokines are found in the joints of rheumatoid arthritis patients, and the cytokines trigger arthritis when applied into the joints of naïve mice. HMGB1 is actively released from immune cells in response to TNFα; once released, HMGB1 in turn induces production of several proinflammatory cytokines – including IL-6 and TNFα – by macrophages. Whether HMGB1-induced arthritis is mediated via the TNFα pathway, however, is unknown. The purpose of the present study was to investigate whether the arthritis-inducing effect of HMGB1 is dependent on TNFα expression in vivo and to assess whether TNFα deficiency affects a proinflammatory cytokine response to HMGB1 in vitro.

Methods
TNFα knockout mice and backcrossed control animals on a C57Bl6 background were injected intraarticularly with 5 μg HMGB1. Joints were dissected 3 days after intraarticular injection and were evaluated histologically by scoring the frequency and severity of arthritis. For in vitro studies, mouse spleen cultures from TNFα knockout mice and from control mice were incubated with different doses of HMGB1, and cell culture supernatants were collected at different time points for analysis of IL-6.

Results
Intraarticular injection of HMGB1 into healthy mouse joints resulted in an overall frequency of 32% to 39% arthritic animals. No significant differences were found with respect to the severity and incidence of synovitis between mice deficient for TNFα (seven out of 18 mice with arthritis) in comparison with control TNFα+/+ animals (six out of 19). No significant differences were detected between spleen cells from TNFα+/+ mice versus TNFα-/- mice regarding IL-6 production upon stimulation with highly purified HMGB1 after 24 hours and 48 hours. Upon stimulation with a suboptimal dose of recombinant HMGB1, however, the splenocytes from TNFα+/+ animals released significantly more IL-6 than cells from the knockout mice (602 ± 112 pg/ml and 304 ± 50 pg/ml, respectively; P < 0.05).

Conclusion
Our data show that HMGB1-triggered joint inflammation is not mediated via the TNF pathway. Combined with our previous study, we suggest that HMGB1-triggered arthritis is probably mediated through IL-1 activation.
Adipose-immune interactions during obesity and caloric restriction: reciprocal mechanisms regulating immunity and health span
Authors: Dixit Vishwa Deep 
Published: June 2008

AbstractIncreasing evidence suggests a tight coupling of metabolic and immune systems. This cross-talk mediated by neuroendocrine peptides as well as numerous cytokines and chemokines is believed to be responsible for integrating energy balance to immune function. These neuroendocrine-immune interactions are heightened during the state of chronic positive energy balance, as seen during obesity, and negative energy balance caused by caloric restriction (CR). Emerging evidence suggests that obesity may be associated with an immunodeficient state and chronic inflammation, which contribute to an increased risk of premature death. The direct interactions between expanded leukocyte populations within the adipose tissue during obesity and an increased number of adipocytes within an aging lymphoid microenvironment may constitute an important adaptive or pathological response as a result of change in energy balance. In stark contrast to obesity, CR causes negative energy balance and robustly prolongs a healthy lifespan in all of the species studied to date. Therefore, the endogenous neuroendocrine-metabolic sensors elevated or suppressed as a result of changes in energy balance may offer an important mechanism in understanding the antiaging and potential immune-enhancing nature of CR. Ghrelin, one such sensor of negative energy balance, is reduced during obesity and increased by CR. Ghrelin also regulates immune function by reducing proinflammatory cytokines and promotes thymopoiesis during aging and thus, may be a new CR mimetic target. The identification of immune effects and molecular pathways used by such orexigenic metabolic factors could offer potentially novel approaches to enhance immunity and increase healthy lifespan.
The diagnostic value of serum and urinary NT-proBNP for heart failure
Authors: Michielsen Etienne C H J , Bakker Jaap A , Kimmenade Roland R J Van , Pinto Yigal M , Dieijen-Visser Marja P Van 
Published: June 2008

Background Serum B-type natriuretic peptide (BNP) and the amino-terminal cleavage product of the prohormone (NT-proBNP) have been shown to be valuable parameters for the diagnosis of heart failure (HF) in the general population. Urinary BNP and NT-proBNP have also been suggested for diagnosis of HF. The present study investigated the diagnostic value of both serum and urinary NT-proBNP in selected groups of controls and patients diagnosed with HF. Methods Creatinine clearance and serum and urinary NT-proBNP were measured in 76 controls and in 47 patients diagnosed with HF (NYHA III and IV). Echocardiography was used to exclude cardiac dysfunction in the control population by the combined normality of left ventricular ejection fraction (LVEF), E/A ratio (echocardiographic early [E] and late, or atrial [A] phases of ventricular filling), deceleration time and LV mass index. All patients diagnosed with HF had LVEF <40%. Results NT-proBNP measurements in urine samples are subject to high variability. Receiver-operating characteristic area under the curve (AUC) for serum, urinary NT-proBNP and their products were 0.94, 0.72 and 0.93, respectively. Correction of urinary NT-proBNP for urinary creatinine content improved the AUC from 0.72 to 0.80. Negative predictive values for ruling out HF were 0.94, 0.67 and 0.89, respectively. Linear regression analysis revealed that creatinine clearance was more important in determining serum NT-proBNP concentrations than age. Conclusions Serum NT-proBNP is the best parameter to rule out HF. The product of the serum and urinary concentrations has equal value. Urinary NT-proBNP alone performs rather poorly. Renal function influences NT-proBNP concentrations more than age in this selected population.