Do nonclinical checkers exhibit deficits in cognitive control? Tests of an inhibitory control hypothesis

We tested the hypothesis that persons who engage in compulsive checking may do so to compensate for cognitive errors produced by deficient inhibitory control. In two experiments, undergraduates were classified by scores on the MOCI checking subscale as checkers or noncheckers. On self-report measures, checkers were significantly more depressed, more anxious, more prone to cognitive slips, and more likely to engage in obsessive-compulsive behaviors. However, checkers performed similarly to noncheckers on laboratory tests of inhibitory control of cognition. Checkers and noncheckers were equally able to (1) ignore distractors in a selective attention task, (2) suppress inappropriate word meanings in a sentence comprehension task, and (3) inhibit retrieval of to-be-forgotten items in a memory task. These results suggest that compulsive checking does not arise from failures of inhibitory control of cognition.     

Recent developments in fuel‐processing and proton‐exchange membranes for fuel cells

In recent years, great progress has been made in the development of proton‐exchange membrane fuel cells (PEMFCs) for both mobile and stationary applications. This review covers two types of new membranes: (1) carbon dioxide‐selective membranes for hydrogen purification and (2) proton‐exchange membranes; both of these are crucial to the widespread application of PEMFCs. On hydrogen purification for fuel cells, the new facilitated transport membranes synthesized from incorporating amino groups in polymer networks have shown high CO₂ permeability and selectivity versus H₂. The membranes can be used in fuel processing to produce high‐purity hydrogen (with less than 10 ppm CO and 10 ppb H₂S) for fuel cells. On proton‐exchange membranes, the new sulfonated polybenzimidazole copolymer‐based membranes can outperform Nafion^® under various conditions, particularly at high temperatures and low relative humidities. Copyright © 2010 Society of Chemical Industry     

Modal Properties of an Index Guiding Nematic Liquid Crystal Based Photonic Crystal Fiber

This paper presents the results of the modal analysis of an index guiding soft glass photonic crystal fiber infiltrated with a nematic liquid crystal (NLC-PCF). The modal analysis is carried out using the full vectorial finite difference method which is capable of dealing accurately with anisotropic waveguide problems. The analyzed parameters are the effective index, birefringence, dispersion, effective mode area, and confinement losses for the two fundamental polarized modes. The effects of the structure geometrical parameters, rotation angle of the director of the NLC and temperature on the modal properties are investigated. The numerical results reveal that the proposed design offers high birefringence of 0.012 at the operating wavelength 1.55 mum with low losses for the two polarized modes. In addition, the structure is tailored to obtain a flat dispersion over a wide range of wavelengths with high birefringence.     

Cranial actinomycosis

A 67-year-old man presented with actinomycotic osteomyelitis of the skull and underlying central nervous system (CNS) involvement. The computed tomography (CT) and magnetic resonance imaging (MRI) findings are discussed and the radiological literature is reviewed.     

Specificity and promiscuity among naturally processed peptides bound to HLA-DR alleles

Naturally processed peptides were acid extracted from immunoaffinity-purified HLA-DR2, DR3, DR4, DR7, and DR8. Using the complementary techniques of mass spectrometry and Edman microsequencing, > 200 unique peptide masses were identified from each allele, ranging from 1,200 to 4,000 daltons (10-34 residues in length), and a total of 201 peptide sequences were obtained. These peptides were derived from 66 different source proteins and represented sets nested at both the amino- and carboxy-terminal ends with an average length of 15-18 amino acids. Strikingly, most of the peptides (> 85%) were derived from endogenous proteins that intersect the endocytic/class II pathway, even though class II molecules are thought to function mainly in the presentation of exogenous foreign peptide antigens. The predominant endogenous peptides were derived from major histocompatibility complex-related molecules. A few peptides derived from exogenous bovine serum proteins were also bound to every allele. Four prominent promiscuous self-peptide sets (capable of binding to multiple HLA-DR alleles) as well as 84 allele-specific peptide sets were identified. Binding experiments confirmed that the promiscuous peptides have high affinity for the binding groove of all HLA-DR alleles examined. A potential physiologic role for these endogenous self-peptides as immunomodulators of the cellular immune response is discussed.     

Raf-1/bcl-2 phosphorylation: a step from microtubule damage to cell death

Carbohydrates comprise an extremely important class of biological molecules but little is known about how they mediate their effects. This gap in understanding is largely due to the fact that obtaining pure carbohydrates in amounts large enough for biochemical studies is extremely difficult. The advent of combinatorial strategies to make carbohydrates promises to revolutionize the field of carbohydrate chemistry and biochemistry.     

Molecular epidemiological analysis of quinolone-resistant Escherichia coli causing bacteremia in neutropenic patients with leukemia in Korea

We analyzed an outbreak of Escherichia coli bacteremia in eight patients with leukemia in a hematology-oncology unit from July to September 1994. The antibiograms and genotypic patterns of the isolates were different, thus suggesting that the outbreak did not originate from a single clone. However, all the isolates were resistant to quinolones, which led us to examine the microbiological records from 1992 to 1994. The incidence of quinolone-resistant E. coli bacteremia in the hematology-oncology unit ranged from 81.8% to 94.6% during this period. We then analyzed 36 more isolates recovered from late 1994 to 1995. Field inversion gel electrophoresis patterns of these isolates were also different. Analysis of the quinolone resistance determining region in gyrA revealed that all the isolates had a double mutation in gyrA. In conclusion, quinolone-resistant E. coli could be an emerging threat to neutropenic patients with leukemia who receive a quinolone prophylactically, and attention must be paid to this trend of resistance.     

IL-1-induced iNOS expression in human astrocytes via NF-kappa B

Nitric oxide (NO) plays an important role in host defense as well as cell injury within the CNS. In contrast to rodent species, human astrocytes are the major glial source of NO. Although interleukin (IL)-1 stimulates astrocyte inducible NO synthase (iNOS) expression, the mechanism is poorly defined. In the present study using primary human fetal astrocyte cultures, we found that IL-1 beta stimulated activation of nuclear factor kappa B (NF-kappa B) within 2 h, iNOS mRNA expression at 8 h, and maximal NO production by 5 days post-treatment. This IL-1-induced activation of astrocyte iNOS was suppressed by pyrrolidine dithiocarbamate, an inhibitor of NF-kappa B activation, suggesting involvement of a NF-kappa B mechanism.     

Zebrafish organizer development and germ-layer formation require nodal-related signals

The vertebrate body plan is established during gastrulation, when cells move inwards to form the mesodermal and endodermal germ layers. Signals from a region of dorsal mesoderm, which is termed the organizer, pattern the body axis by specifying the fates of neighbouring cells. The organizer is itself induced by earlier signals. Although members of the transforming growth factor-beta (TGF-beta) and Wnt families have been implicated in the formation of the organizer, no endogenous signalling molecule is known to be required for this process. Here we report that the zebrafish squint (sqt) and cyclops (cyc) genes have essential, although partly redundant, functions in organizer development and also in the formation of mesoderm and endoderm. We show that the sqt gene encodes a member of the TGF-beta superfamily that is related to mouse nodal. cyc encodes another nodal-related proteins, which is consistent with our genetic evidence that sqt and cyc have overlapping functions. The sqt gene is expressed in a dorsal region of the blastula that includes the extraembryonic yolk syncytial layer (YSL). The YSL has been implicated as a source of signals that induce organizer development and mesendoderm formation. Misexpression of sqt RNA within the embryo or specifically in the YSL induces expanded or ectopic dorsal mesoderm. These results establish an essential role for nodal-related signals in organizer development and mesendoderm formation.     

Possible control of cell death pathways in ataxia telangiectasia. A case report

Peripheral blood monocytes (PBMCs) obtained from a boy with the neuroimmunodegenerative syndrome of ataxia telangiectasia (AT) failed to aggregate or replicate efficiently when mitogenically activated under serum-depleted conditions. These cells rapidly swelled, then slowly shrank, and flattened as they excreted vesicles containing chromatin. This accelerated cell death with loss of homoadhesiveness could be prevented in vitro in most of the homozygous PBMCs by adding large amounts of autologous serum or by adding mixtures of Th1 cytokines, serum factors, and redox agents. However, even in high-serum media containing added cytokines, 20-30% of the homozygous PBMCs quickly flattened, produced minicells, and died. Since the defective functions of the human ataxia-telangiectasia nuclear kinase gene (ATM) could be bypassed in vitro in these defective AT PMBCs by addition of appropriate cytokines and redox survival factors, it may be possible to slow the progressive losses of ATM-deficient lymphoid cells seen in vivo. Since the neuronal degeneration in AT, as seen in the retrovirus-induced neuroimmunodegenerative syndromes, may also be a consequence of impairment of the central and peripheral immune system, it may become possible to prevent the neurodegeneration in AT by using signaling therapies that upregulate the ATM-induced signal deficiencies in the developing immune system.