bluuebunny/crossref_metadata_2025_split huggingface dataset:
Logarithmic phase Escherichia coli K1 efficiently avoids serum killing by promoting C4bp‐mediated C3b and C4b degradation
Authors: Wooster David G. , Maruvada Ravi , Blom Anna M. , Prasadarao Nemani V. 
Published: February 2006

SummaryMeningitis caused by Escherichia coli K1 is a serious illness in neonates with neurological sequelae in up to 50% of survivors. A high degree of bacteremia is required for E. coli K1 to cross the blood–brain barrier, which suggests that the bacterium must evade the host defence mechanisms and survive in the bloodstream. We previously showed that outer membrane protein A (OmpA) of E. coli binds C4b‐binding protein (C4bp), an inhibitor of complement activation via the classical pathway. Nevertheless, the exact mechanism by which E. coli K1 survives in serum remains elusive. Here, we demonstrate that log phase (LP) OmpA+E. coli K1 avoids serum bactericidal activity more effectively than postexponential phase bacteria. OmpA–E. coli cannot survive in serum grown to either phase. The increased serum resistance of LP OmpA+E. coli is the result of increased binding of C4bp, with a concomitant decrease in the deposition of C3b and the downstream complement proteins responsible for the formation of the membrane attack complex. C4bp bound to E. coli K1 acts as a cofactor to factor I in the cleavage of both C3b and C4b, which shuts down the ensuing complement cascade. Accordingly, a peptide corresponding to the complement control protein domain 3 of C4bp sequence, was able to compete with C4bp binding to OmpA and cause increased deposition of C3b. Thus, binding of C4bp appears to be responsible for survival of E. coli K1 in human serum.
Phenotypic and functional characterization of human CD25+ B cells
Authors: Brisslert Mikael , Bokarewa Maria , Larsson Pia , Wing Kajsa , Collins L. Vincent , Tarkowski Andrej 
Published: February 2006

SummaryWe demonstrate that humans have a phenotypically and functionally distinct subset of B lymphocytes that express the interleukin (IL)‐2 receptor (IL‐2R) α‐chain, cluster of differentiation (CD) 25. We found that one‐third of the circulating CD20+ B cells expressed CD25 and, using fluorescence‐activated cell sorter (FACS) analysis, that these cells were significantly larger and more granulated than B cells not expressing CD25. The simultaneous expression of the other two subunits (CD122 and CD132) and the proliferative responses of cells expressing CD25 to IL‐2 suggested that, in addition to CD25, functional IL‐2 receptors were expressed on this cell population. CD25 expression on B cells was selectively up‐regulated by Toll‐like receptor 2 (TLR2), TLR4, and TLR9 ligands but not by a TLR3 ligand or Epstein–Barr virus (EBV) stimulation. Blockade of the nuclear factor (NF)‐κB pathway completely abolished CD25 up‐regulation by these B cells. Interestingly, CD25+ B cells expressed significantly higher levels of surface immunoglobulins but lacked the ability to secrete immunoglobulin (Ig), as compared with CD25− B cells. Furthermore, CD25+ B cells performed significantly better as antigen‐presenting cells in allogeneic mixed lymphocyte reactions (MLR), which may be a result of their expression of high levels of the costimulatory molecules CD27 and CD80. Finally, blocking of CD25 on B cells led to an almost total abrogation of MLR. Our results indicate that CD25+ B cells have distinct phenotypic and functional properties, including the ability to contribute to antigen presentation, which is linked to their expression of CD25. Finally, the differential regulation of CD25 expression via selective TLR ligands suggests a role for CD25+ B cells in bridging innate and acquired immune responses.
Diversified bursal medullary B cells survive and expand independently after depletion following neonatal infectious bursal disease virus infection
Authors: Withers David R. , Davison T. Fred , Young John R. 
Published: February 2006

SummaryThe primary immunoglobulin repertoire of chickens is generated not by gene rearrangement but by a subsequent process of gene conversion in proliferating immature B cells within the follicles of a specialized gut‐associated lymphoid organ, the bursa of Fabricius. Neonatal infection with infectious bursal disease virus can eliminate almost the entire bursal B‐cell compartment. Thereafter, two types of follicle reappear. Larger follicles, with rapidly proliferating B cells and normal structure, are correlated with partial recovery of antibody response. Smaller follicles, lacking distinct cortex and medulla, appear unable to produce antigen‐responsive B cells. To understand the genesis of the two types of follicle, we analysed their VL sequences and activation‐induced deaminase mRNA levels. The results provide a model of bursal repopulation in which surviving bursal stem cells generate new follicles with normal morphology and function, while surviving medullary B cells continue to proliferate slowly, under the influence of stromal cells, giving rise to the smaller follicles. The latter remain fixed in a stage of development incapable of further gene diversification.
Interferon‐αβ mediates partial control of early pulmonary Mycobacterium bovis bacillus Calmette–Guérin infection
Authors: Kuchtey John , Fulton Scott A. , Reba Scott M. , Harding Clifford V. , Boom W. Henry 
Published: February 2006

SummaryThe role of type I interferon (IFN‐αβ) in modulating innate or adaptive immune responses against mycobacterial infection in the lung is unclear. In this study we investigated the susceptibility of IFN‐αβ‐receptor‐deficient (IFN‐αβR–/–) mice to pulmonary infection with aerosolized Mycobacterium bovis bacillus Calmette–Guérin (BCG). During early infection (2–3 weeks), enhanced growth of BCG was measured in the lungs of IFN‐αβR–/– mice compared to wild‐type mice. However, during late infection the burden of BCG was similar in the lungs of IFN‐αβR–/– and wild‐type mice. Although control of BCG growth was delayed, recruitment and activation of T and natural killer cells, production of IFN‐γ, and cytokine expression were all similar in wild‐type and IFN‐αβR–/– mice. However, decreased expression of nitric oxide in bronchoalveolar lavage fluids from IFN‐αβR–/– mice correlated with enhanced growth of BCG. Bone marrow‐derived macrophages from IFN‐αβR–/– mice also produced less nitric oxide following infection with BCG in vitro. These findings suggest that IFN‐αβ contributes to innate immunity to pulmonary mycobacterial infection by augmenting production of nitric oxide.
Risk factors for testicular cancer – differences between pure non‐seminoma and mixed seminoma/non‐seminoma?
Authors: Aschim E. L. , Haugen T. B. , Tretli S. , Daltveit A. K. , Grotmol T. 
Published: February 2006

SummaryThe origin of testicular germ cell cancer (TGCC) is believed to be carcinoma in situ cells developed in utero. Clinically, TGCCs are divided into two major histological groups, seminomas and non‐seminomas, where the latter group includes non‐seminomatous TGCCs with seminomatous components (mixed S/NS TGCC). Recent studies, however, have suggested that non‐seminomas and mixed S/NS TGCCs could have certain differences in aetiology, and in this study the TGCCs were divided into three, rather than the conventional two histological groups. A large case‐control study was undertaken on data on all live‐born boys registered in the Medical Birth Registry of Norway during the period 1967–1998 (n = 961 396). Among these were 1087 TGCC cases registered in the Cancer Registry of Norway until February 2004. We found several risk factors for TGCC, including low parity, low gestational age, epilepsy and retained placenta. Several of the variables studied seemed to be risk factors for specific histological groups, e.g. parity 0 vs. 2 and low gestational age being associated with increased risk of non‐seminomas, but not of mixed S/NS TGCC, and low maternal age being associated with increased risk of mixed S/NS TGCC, but not of non‐seminomatous TGCC. Therefore, our results might suggest that non‐seminomas and mixed S/NS TGCCs have partially different risk factors, whose associations may be obscured by combining these two histological groups. The histological groups were not significantly different, however. Most of our findings on risk factors for TGCC are in agreement with at least some previous studies. An unexplainable exception is low birth weight being associated with reduced risk of TGCC in our study.
Molecular analysis of polymerase gamma gene and mitochondrial polymorphism in fertile and subfertile men
Authors: Harris T. P. , Gomas K. P. , Weir F. , Holyoake A. J. , McHugh P. , Wu M. , Sin Y. , Sin I. L. , Sin F. Y. T. 
Published: February 2006

SummaryCAG trinucleotide repeat length in the nuclear polymerase gamma gene (POLγ) has been shown to be associated with men with reduced fertility. The present study investigated the frequency of CAG repeat length genotypes and three exonuclease motifs of the POLγ in relation to the frequency of mitochondrial nucleotide substitutions. DNA from semen samples of 93 normozoospermic men and 192 non‐normozoospermic men was isolated and the specific regions of the genes were amplified by polymerase chain reactions (PCR) and sequenced to identify mutations. The genotypic frequencies of pooled POLγ CAG repeat lengths, =10/≠10 heterozygotes and ≠10/≠10 homozygotes, were significantly different between normozoospermic and non‐normozoospermic men (p < 0.05), with non‐normozoospermic men having a slightly higher frequency of the =10/=10 genotypes. The allelic frequency for =10 is 0.79 and ≠10 is 0.21 for normozoospermic men and 0.85 and 0.15, respectively, for non‐normozoospermic men (p < 0.025). There was no mutation detected in the exonuclease motifs in all the samples tested. Eighty normozoospermic and 124 non‐normozoospermic semen samples were analysed for nucleotide substitutions in mitochondrial genes by PCR and sequencing. Heteroplasmic mutations were found in one azoospermic man, four asthenozoospermic men and two normozoospermic men. Only one asthenozoospermic man was heterozygous for the POLγ genotype. Of the 17 men with non‐synonymous nucleotide substitutions, 14 were homozygous for the POLγ genotype. Non‐normozoospermic men had twice as many nucleotide substitutions than normozoospermic men. However, there were no significant differences in the frequencies of nucleotide substitution and POLγ genotypes in the two groups of men.
Impaired decision making following 49 h of sleep deprivation
Authors: KILLGORE WILLIAM D. S. , BALKIN THOMAS J. , WESENSTEN NANCY J. 
Published: February 2006

SummarySleep deprivation reduces regional cerebral metabolism within the prefrontal cortex, the brain region most responsible for higher‐order cognitive processes, including judgment and decision making. Accordingly, we hypothesized that two nights of sleep loss would impair decision making quality and lead to increased risk‐taking behavior on the Iowa Gambling Task (IGT), which mimics real‐world decision making under conditions of uncertainty. Thirty‐four healthy participants completed the IGT at rested baseline and again following 49.5 h of sleep deprivation. At baseline, volunteers performed in a manner similar to that seen in most samples of healthy normal individuals, rapidly learning to avoid high‐risk decks and selecting more frequently from advantageous low‐risk decks as the game progressed. After sleep loss, however, volunteers showed a strikingly different pattern of performance. Relative to rested baseline, sleep‐deprived individuals tended to choose more frequently from risky decks as the game progressed, a pattern similar to, though less severe than, previously published reports of patients with lesions to the ventromedial prefrontal cortex. Although risky decision making was not related to participant age when tested at rested baseline, age was negatively correlated with advantageous decision making on the IGT, when tested following sleep deprivation (i.e. older subjects made more risky choices). These findings suggest that cognitive functions known to be mediated by the ventromedial prefrontal cortex, including decision making under conditions of uncertainty, may be particularly vulnerable to sleep loss and that this vulnerability may become more pronounced with increased age.
Sleep hygiene and actigraphically evaluated sleep characteristics in children with ADHD and chronic sleep onset insomnia
Authors: VAN DER HEIJDEN KRISTIAAN B. , SMITS MARCEL G. , GUNNING W. BOUDEWIJN 
Published: February 2006

SummaryIn the present study we investigated sleep hygiene and actigraphically evaluated sleep in 74 medication‐naïve children, aged 6–12 years, with rigorously diagnosed attention‐deficit/hyperactivity disorder (ADHD) and chronic sleep onset insomnia (ADHD‐SOI) and 23 ADHD controls without insomnia (ADHD‐noSOI). Between‐group differences were analysed for lights out (sleep log), actigraphically evaluated sleep onset, sleep latency, total sleep duration, actual sleep time and sleep hygiene as measured with the Children's Sleep Hygiene Scale. We found a significant difference (P < 0.001) in mean (±SD) sleep onset between the ADHD‐SOI group (21:49 ± 0:56 h) and ADHD‐noSOI groups (20:41 ± 0:45 h). Sleep latency was significantly (P < 0.001) longer in ADHD‐SOI (00:53 ± 0:25 h) compared to ADHD‐noSOI (00:26 ± 0:25 h). The difference in total sleep duration between ADHD‐SOI (9:42 ± 0:44 h) and ADHD‐noSOI (10:09 ± 0:43 h) was not significantly different (P = 0.18). The group difference in actual sleep time was also not significant (8:43 ± 0:52 h in ADHD‐SOI versus 9:13 ± 1:16 h; P = 0.40). There was no significant difference (P = 0.17) in mean (±SD) total sleep hygiene score between the ADHD‐SOI (56.4 ± 10.5) and ADHD‐noSOI groups (53.0 ± 10.6). We conclude that there were differences in sleep onset and sleep latency in ADHD children with chronic SOI and those without insomnia; however, sleep hygiene practices were similar and did not relate to sleep characteristics.
Fatigue and shift work
Authors: SHEN JIANHUA , BOTLY LEIGH C. P. , CHUNG SHARON A. , GIBBS ALISON L. , SABANADZOVIC SKENDER , SHAPIRO COLIN M. 
Published: February 2006

SummaryShift work is a ubiquitous phenomenon and its adverse effects on workers’ physical and mental health have been documented. In the sleep literature, differentiating between the symptoms of fatigue and sleepiness, and developing appropriate objective and subjective measures, have become very important endeavors. From such research, fatigue and sleepiness have been shown to be distinct and independent phenomena. However, it is not known whether shift work differentially affects fatigue and sleepiness. In an attempt to answer this question, 489 workers from a major Ontario employer completed a series of subjective, self‐report questionnaires, including the Fatigue Severity Scale (FSS) and the Epworth Sleepiness Scale. Workers were separated into four groups based on the frequency with which they are engaged in shift work (never, fewer than four times per month, 1–2 days per week, 3 days or more per week). The frequency of shift work was found to have a significant effect on subjective fatigue, but not on subjective sleepiness. Compared with the subjects who never had a shift schedule, those who worked in a shift for 3 days or more had significantly higher mean score of the FSS. In agreement with previous results, a low correlation was found between workers’ subjective fatigue and sleepiness scores, providing further support for the concept of fatigue and sleepiness as distinct and independent phenomena. Future research should address the possibility of using the FSS as an indicator when the frequency of shift work has become high enough to adversely affect work performance or cause health problems.
Sleep‐disordered breathing in a general heart failure population: relationships to neurohumoral activation and subjective symptoms
Authors: RAO ARCHANA , GEORGIADOU PANAGIOTA , FRANCIS DARREL P. , JOHNSON ANDREW , KREMASTINOS DIMITRIS TH. , SIMONDS ANITA K. , COATS ANDREW J. S. , COWLEY ALAN , MORRELL MARY J. 
Published: February 2006

SummaryThe aim of this study was to determine the prevalence of sleep‐related breathing disorders (SDB) in a UK general heart failure (HF) population, and assess its impact on neurohumoral markers and symptoms of sleepiness and quality of life. Eighty‐four ambulatory patients (72 male, mean (SD) age 68.6 (10) yrs) attending UK HF clinics underwent an overnight recording of respiratory impedance, SaO2 and heart rate using a portable monitor (Nexan). Brain natriuretic peptide (BNP) and urinary catecholamines were measured. Subjective sleepiness and the impairment in quality of life were assessed (Epworth Sleepiness Scale (ESS), SF‐36 Health Performance Score). SDB was classified using the Apnoea/Hypopnoea Index (AHI). The prevalence of SDB (AHI > 15 events h−1) was 24%, increasing from 15% in mild‐to‐moderate HF to 39% in severe HF. Patients with SDB had significantly higher levels of BNP and noradrenaline than those without SDB (mean (SD) BNP: 187 (119) versus 73 (98) pg mL−1, P = 0.02; noradrenaline: 309 (183) versus 225 (148) nmol/24 h, P = 0.05). There was no significant difference in reported sleepiness or in any domain of SF‐36, between groups with and without SDB (ESS: 7.8 (4.7) versus 7.5 (3.6), P = 0.87). In summary, in a general HF clinic population, the prevalence of SDB increased with the severity of HF. Patients with SDB had higher activation of a neurohumoral marker and more severe HF. Unlike obstructive sleep apnoea, SDB in HF had little discernible effect on sleepiness or quality of life as measured by standard subjective scales.
Random number generation during sleep deprivation: effects of caffeine on response maintenance and stereotypy
Authors: GOTTSELIG JULIE M. , ADAM MARTIN , RÉTEY JULIA V. , KHATAMI RAMIN , ACHERMANN PETER , LANDOLT HANS‐PETER 
Published: February 2006

SummaryNeurophysiological and functional imaging studies have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure. Previous neuropsychological studies indicate that sleep deprivation causes impairments in prefrontal cortical function. Random number generation (RNG) is thought to provide a sensitive index of executive functions that rely on the prefrontal cortex. The present study tested the hypothesis that sleep deprivation would impair RNG and that caffeine would mitigate this impairment. Healthy young men (n = 21) participated in two 40‐h sleep deprivations 1 week apart. During each sleep deprivation period subjects received either caffeine or placebo according to a randomized, double‐blind cross‐over design, and they completed an oral RNG task at 3‐h intervals. Comparison of test sessions at analogous times of day revealed that sleep deprivation was associated with significant drops in the number of responses, a threefold increase in the percentage of rule violations, 59% greater response redundancy and a 20% increase in stereotypy of adjacent response pairs. Sleep deprivation did not consistently alter counting tendency. Caffeine ameliorated the decrease in the number of responses but did not mitigate other deficits in RNG that arose during sleep deprivation. These findings are consistent with prior reports of diminished vigilance and increased perseveration during extended wakefulness. They support the conclusion that caffeine preserves simple aspects of cognitive performance during sleep deprivation, whereas caffeine may not prevent detrimental effects of sleep deprivation on some complex cognitive functions.
Circulating adrenomedullin in obstructive sleep apnoea
Authors: SCHULZ RICHARD , FLÖTOTTO CHRISTIANE , JAHN ANDREAS , EISELE HANS JOACHIM , WEISSMANN NORBERT , SEEGER WERNER , ROSE FRANK 
Published: February 2006

SummaryAdrenomedullin (AM) is a potent endothelial‐derived vasodilator secreted under the influence of various stimuli such as hypoxia, shear stress and cytokines. As all of these stimuli might be active under the conditions of obstructive sleep apnoea (OSA), we hypothesized that vascular AM production is increased in these patients. The study included 41 consecutive OSA patients and 28 control subjects without sleep‐disordered breathing who were recruited from a pool of patients hospitalized for other reasons. Both groups were matched for anthropometric and comorbid factors. In all patients, i.e. OSA and controls, peripheral venous blood samples were taken at 07:00 hours after diagnostic polysomnography. In subsets of OSA patients, this was repeated after two nights of continuous positive airway pressure (CPAP) therapy (n = 28) and after several months of constant CPAP use (n = 11). The controls and the untreated OSA patients did not have serial blood sampling. In all blood samples, plasma AM levels were measured by an enzyme immunoassay kit. At baseline, the OSA patients had markedly elevated AM concentrations when compared to the controls. There were no differences between normo‐ and hypertensive OSA patients. After two nights of CPAP therapy, AM levels significantly decreased. Patients on long‐term CPAP treatment showed complete normalization of plasma AM concentrations. In conclusion, this pilot study suggests that circulating AM is increased in untreated OSA irrespective of coexistent arterial hypertension and declines after CPAP therapy. AM upregulation might be considered as an adaptive mechanism to counteract the emergence of OSA‐related cardiovascular disease.
Characterizing sleep problems in persons with Alzheimer's disease and normal elderly
Authors: TRACTENBERG ROCHELLE E. , SINGER CLIFFORD M. , KAYE JEFFREY A. 
Published: February 2006

SummaryWe retrospectively analyzed sleep disturbance symptoms and estimated time in bed from the intake interviews of 399 healthy, non‐demented elderly (NDE) and 263 persons with a diagnosis of possible (n = 53) or probable (n = 210) Alzheimer's disease (AD). Our primary objective was to identify what symptoms might underlie an individual's perception of ‘sleep problems’ and to determine if these were consistent within, and across, our two cohorts. We stratified each cohort according to whether or not they (or their caregiver) indicated that they had a ‘sleep problem’, and compared the frequency and endorsement rates of each of 21 sleep disturbance symptoms across those who did or did not endorse ‘sleep problem’. For less than half of the symptoms in persons with AD, and a quarter of those in NDE, endorsement rates were significantly different depending on whether the reporter (or their sleep partner) did or did not report a sleep problem. Differences in mean frequency ratings between individuals reporting sleep problems relative to those not reporting were observed on 10 symptoms in both cohorts; six of these were the same symptom for both cohorts. When persons with subjective sleep problems in the AD and NDE cohorts were compared, only four of 21 symptoms were endorsed in one and not the other; two symptoms were significantly more frequent in one cohort than the other. Thus, within cohorts, the differences between persons with and without ‘sleep problems’ were relatively pronounced while the main differences in specific sleep‐related symptoms between AD and NDE were not. Observed between‐cohort differences appear to be driven by who is reporting, and the high prevalence of daytime sleeping in AD. Within‐cohort differences reflect a clear distinction between persons with and without sleep problems, regardless of the reporter.