bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accumulation of human immunodeficiency virus‐specific cytotoxic T lymphocytes away from the predominant site of virus replication during primary infection
Authors: Pantaleo Giuseppe , Soudeyns Hugo , Demarest James F. , Vaccarezza Mauro , Graziosi Cecilia , Paolucci Stefania , Daucher Marybeth , Cohen Oren J. , Denis François , Biddison William E. , Sekaly Rafick P. , Fauci Anthony S. 
Published: March 2007

AbstractDown‐regulation of the initial burst of viremia during primary human immunodeficiency virus (HIV) infection is thought to be mediated predominantly by HIV‐specific CD8+ cytotoxic T lymphocytes (CTL). This response is associated with major perturbations in the T cell receptor (TCR) repertoire. To investigate the failure of the cellular immune response to adequately control viral spread and replication and to prevent establishment of HIV infection, changes in the TCR repertoire and in the distribution of virus‐specific CTL between blood and lymph node were analyzed in three patients with primary infection. By the combined use of clonotype‐specific polymerase chain reaction and analysis of the frequency of in vivo activated HIV‐specific CTL, it was shown that HIV‐specific CTL clones preferentially accumulated in blood as opposed to lymph node. Accumulation of HIV‐specific CTL in blood occurred prior to effective downregulation of virus replication in both blood and lymph node. These findings should provide new insights into how HIV, and possibly other viruses, elude the immune response of the host during primary infection.
Cloning of a mouse homolog of CD94 extends the family of C‐type lectins on murine natural killer cells
Authors: Vance Russell E. , Tanamachi Dawn M. , Hanke Thomas , Raulet David H. 
Published: March 2007

AbstractTwo families of major histocompatibility complex (MHC) class I‐specific receptors are found on natural killer (NK) cells: immunoglobulin‐like receptors and C‐type lectin receptors. In mice, the latter category is represented by the Ly49 family of receptors, whereas in humans, NK cells express the distantly related CD94, which forms MHC class I‐specific heterodimers with NKG2 family members. Humans also express the MHC class I‐specific p50/p58/p70 family of immunoglobulin‐like receptors, but these have not been identified in mice. Hence, there is no known instance of an MHC class I‐specific receptor that is expressed by both human and murine NK cells. Here we report the cloning of CD94 from the CB.17 and C57BL/6 strains of mice. Mouse CD94 is 54 % identical and 66 % similar to human CD94, and is also a member of the C‐type lectin superfamily. Mouse CD94 is expressed efficiently on the cell surface of cells transiently transfected with the corresponding cDNA, but surface CD94 was unable to mediate detectable binding to MHC class I‐expressing ConA blasts. Notably, mouse CD94, like human CD94, has a very short cytoplasmic tail, suggesting the existence of partner chains that may play a role in ligand binding and signaling. Like many other C‐type lectins expressed by NK cells, mouse CD94 maps to the NK complex on distal chromosome 6, synteneic to human CD94. We also demonstrate that mouse CD94 is highly expressed specifically by mouse NK cells, raising the possibility that mice, like humans, express multiple families of MHC class I‐specific receptors on their NK cells. Murine homologs of human NKG2 family members have not yet been identified, but we report here the existence of a murine NKG2D‐like sequence that also maps to the murine NK complex near CD94 and Ly49 family members.
Recruitment, activation and proliferation of CD8+ memory T cells in an immunoprivileged site
Authors: Stevenson Philip G. , Bangham Charles R. M. , Hawke Simon 
Published: March 2007

AbstractThe capacity of a memory cytotoxic T lymphocyte (CTL) population to protect against viral infections is well established, but the processes underlying this protection are less well understood. We have used heterotypic intranasal immunization with influenza A/X31 (H3N2) to protect against a subsequent infection with the neurovirulent influenza A/WSN (H1N1) in either the cerebrospinal fluid or the immunoprivileged brain parenchyma. Viral clearance from both sites was associated with a local infiltration and proliferation of A/WSN‐specific CD8+ T cells. Infection in the cerebrospinal fluid elicited a proliferative response in the draining lymph nodes, an anti‐H1N1 serum antibody response and an increase in the extracerebral A/WSN‐specific CTL precursor frequency. In contrast, infection in the brain parenchyma elicited no lymph node proliferative response or serum antibody response and caused a transient decrease in the extracerebral CTL precursor frequency. Thus the memory CTL population protected against an intracerebral viral infection independent of any immune response occurring in systemic lymphoid tissue.
Lipopolysaccharide complexed with soluble CD14 binds to normal human monocytes
Authors: Blondin Catherine , Le Dur Annick , Cholley Béatrice , Caroff Martine , Haeffner‐Cavaillon Nicole 
Published: March 2007

AbstractUsing flow cytometry we have compared the binding of Neisseria meningitidis lipopolysaccharide labeled with fluorescein isothiocyanate (FITC‐LPS) to normal human monocytes in whole blood with the binding to Chinese hamster ovary (CHO) cells transfected with human CD14 gene (hCD14‐CHO cells). Binding of FITC‐LPS to cells was dose dependent, saturable and enhanced in the presence of increasing concentrations of serum. Blockade of membrane CD14 with saturating concentrations of anti‐CD14 monoclonal antibody (mAb) My4 inhibited 50% of the binding of FITC‐LPS to monocytes and 100% to hCD14‐CHO cells. Similarly, removal of membrane CD14 by phosphatidylinositol phospholipase C (Pl‐PLC) treatment of the cells partially decreased the binding of FITC‐LPS to monocytes but totally inhibited the binding to hCD14‐CHO‐transfected cells. These results suggest that binding of FITC‐LPS to monocytes is not only mediated by membrane CD14. Using two‐color flow cytometry, we observed that FITC‐LPS binds to My4‐saturated monocytes in association with soluble (s)CD14 present in serum as revealed by staining with rhodaminelabeled My4 mAb. The binding of FITC‐LPS/sCD14 complexes to monocytes treated with saturating amounts of unlabeled My4 prior to addition of the complexes was completely inhibited by anti‐CD14 mAb 10G33. When cells were first saturated with a mixture of My4 and 10G33 mAb, washed and further incubated with FITC‐LPS/sCD14, inhibition of the binding of LPS was similar to that observed with cells saturated with My4 alone, showing that the binding of FITC‐LPS is not mediated by the 10G33 epitope present on mCD14. These results suggest that either the 10G33 epitope on sCD14 is involved in the binding of LPS/sCD14 complexes to the cells, or that 10G33 mAb inhibits the binding of FITC‐LPS to sCD14. Taken together, these data indicate that sCD14 which is present in normal serum, in addition to membrane CD14, enables LPS to bind monocytes through an as yet unidentified molecule and that sCD14 does not simply serve as a shuttle for transfer of LPS to membrane CD14.
CD8+ T cells control Th2‐driven pathology during pulmonary respiratory syncytial virus infection
Authors: Hussell Tracy , Baldwin Christopher J. , O'Garra Anne , Openshaw Peter J. M. 
Published: March 2007

AbstractBALB/c mice vaccinated with vaccinia virus expressing the major surface glycoprotein G of respiratory syncytial virus (RSV) develop lung eosinophilia during RSV challenge. The G protein is remarkable in that it induces CD4+, but no CD8+ T cells in this mouse strain. Studies using passive T cell transfers show that co‐injection of CD8+ T cells greatly reduces the Th2‐driven lung eosinophilia caused by G‐specific CD4+ T cells. By contrast, vaccination with the fusion protein (F) induces both CD8+ and CD4+ T cells, but not lung eosinophilia during RSV infection. These observations suggest that CD8+ T cells play a crucial role in preventing Th2‐driven pathology. We therefore depleted mice with anti‐CD8 antibodies in vivo. This treatment allowed lung eosinophilia to develop in F‐primed mice. Depletion of interferon (IFN)‐γ had a similar effect, suggesting that secretion of this cytokine is the mechanism by which CD8+ T cells exert their effect. To test whether similar effects occurred in other strains of mice, RSV‐infected C57BL/6 mice (which do not develop eosinophilia after sensitization to G) were treated with anti‐IFN‐γ. Again, these mice developed eosinophilia. In this strain, genetic deletion of CD8‐α, β2‐microglobulin or genes coding for the transporter associated with antigen presentation (which in each case eliminates CD8+ T cells) caused lung eosinophilia during RSV infection. These studies show the critical roles that CD8+ T cells and IFN‐γ production play in regulating Th2‐driven eosinophilia and provide a unifying explanation for previous studies of lung eosinophilia. We propose that vaccines designed to enhance CD8+ T cell recognition might avoid disease caused by CD4+ Th2 cells.
The nature of the signals regulating CD8 T cell proliferative responses to CD8α+ or CD8α− dendritic cells
Authors: Winkel Kenneth D. , Kronin Vadim , Krummel Matthew F. , Shortman Ken 
Published: March 2007

AbstractThe CD8α−‐expressing dendritic cells (DC) of mouse spleen have been shown to be poor inducers of interleukin (IL)‐2 production by CD8 T cells when compared to the CD8− DC. As a consequence, CD8 T cells give a more prolonged proliferative response to CD8− DC than to CD8+ DC. The possible mechanisms underlying these functional differences in DC subtype have been investigated. Inadequate co‐stimulation did not underlie the poor T cell response to allogeneic CD8+ DC. Equivalent levels of B7‐1 (CD80) and B7‐2 (CD86) were found on the two DC subtypes and co‐stimulator assays did not reveal any functional differences between them. Although CD8+ DC were found to die more rapidly in culture than CD8− DC, this did not explain their reduced stimulatory ability. Neither prolonging DC survival in culture nor renewing the stimulator cells by repeated addition of freshly isolated DC had any significant effect on the T cell responses. Furthermore, later addition to the cultures of DC of the opposite type to the initiating DC did not reverse or eliminate the differential response to the initiating DC. The role of DC‐derived soluble factors was examined by addition to the cultures of supernatants derived from freshly isolated or stimulated DC of the opposite type. This neither enhanced the poor stimulatory capacity of CD8+ DC nor inhibited the stimulation by CD8− DC. Furthermore, addition of a series of cytokines that might have been produced by the DC did not eliminate the differences in T cell proliferation. Only the addition to the cultures of the growth factors IL‐2 and IL‐4 overcame the stimulatory difference between the two DC populations, confirming that the difference in T cell proliferative responses was a consequence of differences in induced cytokine production. The difference in the response of CD8 T cells to CD8+ and CD8− DC is therefore determined by direct DC‐T cell contact during the earliest stages of the culture and involves an undetermined and possibly new signaling system.
Polythiacrown Macro‐ and Gigantocycles with Chiral Diacetal Cores
Authors: Abramson Sarah , Berkovich‐Berger Dvora , Dagan Shai , Goldberg Israel , Golender Lara , Grabarnik Mikhail , Lemcoff N. Gabriel , Weinman Sarah , Fuchs Benzion 
Published: March 2007

AbstractWe present a unique class of polythiacrown macro‐ and gigantocyclic[9] systems, consisting of ethylene 1,2‐dithioglycol (ETG) to poly(ethylene thioglycol) (ETGn) bridges over one to six diacetal units of the cis‐1,3,5,7‐tetraoxadecalin (TOD) type. The latter is a dissymmetric, chiral moiety, incorporating a cavity with built‐in high electron lone pair concentration, serving as the “core” of chiral macrocyclic host systems with good inclusion ability of ions and polar molecules. We describe two approaches: (i) the reactions of the 2,6‐bis(bromomethyl)‐cis‐TOD podand (6) with ETG or higher ETGns (12n), in Cs2CO3 promoted processes, leading to the innate but uncontrolled formation of polythiacrown‐TOD macrocycles having ETG/TOD ratios of 1:1 (7), 2:2 (8) and further 3:3–6:6 (111/m)10 macrocycles via open dithiol intermediates, and (ii) judicious preparation, using K2CO3, of oligomeric dibromide intermediates with ETGn:TOD ratios 1:2, 2:3 or 3:4 (14n/m), which led (with further ETGn) in a controlled way to the 2:2 (8n), or 3:3, 4:4 and 6:6 (11n/m) macro‐ and gigantocyclic systems. Altogether, the outcome of these processes depends on the relative concentrations of the reactants. Synthesis was accompanied by detailed (NMR and MS) spectroscopy. X‐ray crystallographic analysis of a number of macrocycles, complemented by (MM & MD) computation, made possible valuable structural, stereochemical and conformational analysis. While sophisticated in their stereochemical features, these systems are readily prepared in enantiopure form and hold great promise of chemical reactivity in metal ion inclusion and molecular and chiral recognition.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
On the Functionalization of [2.2](1,4)Phenanthrenoparacyclophane
Authors: Hopf Henning , Hucker Joachim , Ernst Ludger 
Published: March 2007

AbstractTwo routes for preparing functionalized [2.2](1,4)phenanthrenoparacyclophanes are described: either the parent system 2 is subjected to electrophilic substitution (bromination, Friedel–Crafts acylation, Rieche formylation: preparation of 5, 6, 7, 11 and 12) or the desired substituents are incorporated in the early stages of the synthesis by the preparation of the corresponding functionalized styryl paracyclophanes and their photocyclization to the respective phenanthrenocyclophanes. By these specific routes various bromides (22a,b), ethers (28a–c) and phenols (29a,b) were synthesized. The latter derivatives, on oxidation, furnish para‐ (31) and ortho‐quinonophanes (30, 32, 33), useful substrates for the preparation of cyclophanes containing phenazine subunits (36). The stilbene → phenanthrene photocyclization can also be employed for the preparation of benzothiophenophanes, e.g. 43 and 44, from the respective precursors. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Pro‐eating disorder websites: users' opinions
Authors: Csipke Emese , Horne Outi 
Published: March 2007

AbstractThe phenomenon of ‘pro‐eating disorder’ websites remains relatively unexplored by researchers in published formats. Supporters of the sites claim beneficial effects but health professionals worry that the sites propagate disordered behaviours. The present study addressed visitor characteristics and perceived impact of visits. A 24‐item questionnaire supplemented with the Eating Attitudes Test‐26 (EAT‐26) was developed and posted on the website of the UK mental health charity SANE. Participants who interacted with others on the sites and sought emotional support reported improved mental state after visiting, and for them, evidence was found of reduced impact from potentially damaging content. ‘Silent browsing’ in order to sustain a disorder was found to be mainly harmful. ‘Silent browsers’ may be particularly vulnerable to a worsening of their symptoms in the absence of beneficial effects from emotional support, but those who interact and find support could face a danger of a different sort. © 2007 John Wiley & Sons, Ltd and Eating Disorders Association.
Making choices between prepayment and user charges in Zambia. What are the results for equity?
Authors: Kondo Masahide , McPake Barbara 
Published: March 2007

AbstractIn many low‐income countries, user charges were introduced in the 1990s. As problems emerged of equity of access, interest grew in developing prepayment mechanisms to protect users from risk of out‐of‐pocket payments. In Zambia, a prepayment scheme did not generate sufficient revenue, due to abuses of its terms. An alternative scheme using discount cards (a set of coupons to cover episodes of care at discount) was devised.We aimed to understand the equity implications of prepayment and discount cards relative to user charges. We proposed models predicting roles of income, perceived health status, perceived quality of care and time preference in choice of payment mechanism and use of health services. We tested these models using three data sets that could be accessed or collected.It is concluded that relative to user charges, prepayment may facilitate access without incurring income‐related equity losses. Evidence concerning discount cards was weaker. We concluded that they facilitate access to a lesser extent.Discount cards offer a credible intermediate solution between user charges and prepayment that avoid some problems associated with prepayment. However, since prepayment seems to be associated with the most positive outcomes, finding other solutions to their problems would be preferred. Copyright © 2007 John Wiley & Sons, Ltd.
Health insurance coverage and the use of preventive services by Mexican adults
Authors: Pagán José A. , Puig Andrea , Soldo Beth J. 
Published: March 2007

AbstractThe lack of health insurance coverage could be a potentially important deterrent to the use of preventive health care by older adults with high rates of chronic co‐morbidities. We use survey data from 12 100 Mexican adults ages 50 and older who participated in the 2001 Mexican Health and Aging Study (MHAS) to analyze the relation between health insurance coverage and the use of preventive health‐care services in Mexico. Uninsured adults were less likely to use preventive screenings for hypertension, high cholesterol, diabetes and (breast, cervical and prostate) cancer than insured adults. After adjusting for other factors affecting preventive care utilization in a logistic regression model, we found that these results still hold for high cholesterol and diabetes screening. Similar results hold for the population not working during the survey week and for adults earning below 200% of the poverty line. Our results suggest that insured adults are in a relatively better position to detect some chronic diseases – and have them treated promptly – than uninsured adults because they have better access to cost‐effective preventive screenings. Recent public policy initiatives to increase health insurance coverage rates in Mexico could lead to substantially higher preventive health‐care utilization rates and improvements in population health. Copyright © 2007 John Wiley & Sons, Ltd.
Presynaptic calcium stores contribute to nicotine‐elicited potentiation of evoked synaptic transmission at CA3‐CA1 connections in the neonatal rat hippocampus
Authors: Le Magueresse Corentin , Cherubini Enrico 
Published: March 2007

AbstractNicotine acetylcholine (ACh) receptors (nAChRs) are ligand‐gated ion channels that are widely expressed throughout the central nervous system. It is well established that presynaptic, α7‐containing nAChRs modulate glutamate release in several brain areas, and that this modulation requires extracellular calcium. However, the intracellular mechanisms consecutive to nAChR opening are unclear. Recent studies have suggested a role for presynaptic calcium stores in the increase of neurotransmitter release following nAChR activation. Using the minimal stimulation protocol at low‐probability Schaffer collateral synapses in acute hippocampal slices from neonatal rats, we show that nicotine acting on presynaptic α7 nAChRs persistently upregulates glutamate release. We tested the role of calcium stores in this potentiation. First, we examined the relationship between calcium stores and glutamate release. We found that bath application of SERCA pump inhibitors (cyclopiazonic acid and thapsigargin), as well as an agonist of ryanodine receptors (ryanodine 2 μM) increases the probability of glutamate release at CA3‐CA1 synapses, decreases the coefficient of variation and the paired‐pulse ratio, indicating that presynaptic activation of calcium‐induced calcium release can modulate glutamatergic transmission. Next, we investigated whether blocking calcium release from internal stores could alter the effect of nicotine. Preincubation with thapsigargin (10 μM), cyclopiazonic acid (30 μM), or with a high (blocking) concentration of ryanodine (100 μM) for 30 min to 5 h failed to block the effect of nicotine. However, after preincubation in ryanodine, nicotine‐elicited potentiation was significantly shortened. These results indicate that at immature Schaffer collateral‐CA1 synapses, activation of presynaptic calcium stores is not necessary for but contributes to nicotine‐elicited increase of neurotransmitter release. © 2007 Wiley‐Liss, Inc.
Steroid pregnenolone sulfate enhances NMDA‐receptor‐independent long‐term potentiation at hippocampal CA1 synapses: Role for L‐type calcium channels and sigma‐receptors
Authors: Sabeti Jilla , Nelson Thomas E. , Purdy Robert H. , Gruol Donna L. 
Published: March 2007

AbstractSevere stress elevates plasma and CNS levels of endogenous neuroactive steroids that can contribute to the influence of stress on memory formation. Among the neuroactive steroids, pregnenolone sulfate (PREGS) reportedly strengthens memories and is readily available as a memory‐enhancing supplement. PREGS actions on memory may reflect its ability to produce changes in memory‐related neuronal circuits, such as long‐term potentiation (LTP) of excitatory transmission in hippocampus. Here, we report a previously undiscovered pathway by which PREGS exposure promotes activity‐dependent LTP of field excitatory postsynaptic potentials at CA1 synapses in hippocampal slices. Thus, application of PREGS, but not the phosphated conjugate of the steroid, selectively facilitates the induction of a slow‐developing LTP in response to high‐frequency (100 Hz) afferent stimulation, which is not induced in the absence of the steroid. The slow‐developing LTP is independent of NMDA‐receptor function (i.e., dAP5 insensitive) but dependent on functional L‐type voltage‐gated calcium channels (VGCC) and sigma‐receptors. By contrast, PREGS at the highest concentration tested produces a depression in NMDA‐receptor‐dependent LTP, which is evident when sigma‐receptor function is compromised by the presence of a sigma‐receptor antagonist. We found that at early times during the induction phase of L‐type VGCC‐dependent LTP, PREGS via sigma‐receptors transiently enhances presynaptic function. As well, during the maintenance phase of L‐type VGCC‐dependent LTP, PREGS promotes a further increase in presynaptic function downstream of LTP induction, as evidenced by a decrease in paired‐pulse facilitation. The identification of complex regulatory actions of PREGS on LTP, involving sigma‐receptors, L‐type VGCCs, NMDA‐receptors, and inhibitory circuits will aid future research endeavors aimed at understanding the precise mechanisms by which this stress‐associated steroid may engage multiple LTP‐signaling pathways that alter synaptic transmission at memory‐related synapses. © 2007 Wiley‐Liss, Inc.