bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trauma-Related Dreams of Australian Veterans with PTSD: Content, Affect and Phenomenology
Authors: Phelps Andrea J. , Forbes David , Hopwood Malcolm , Creamer Mark 
Published: August 2011

Objective: Consensus on the parameters of trauma-related dreams required to meet criteria for post-traumatic stress disorder (PTSD) is critical when: (i) the diagnosis requires a single re-experiencing symptom; and (ii) trauma dreams are prevalent in survivors without PTSD. Method: This study investigated the phenomenology of PTSD dreams in 40 veterans, using structured interview and self-report measures. Results: Dream content varied between replay, non-replay, and mixed, but affect was largely the same as that experienced at the time of trauma across all dream types. ANOVA indicated no difference between dream types on PTSD severity or nightmare distress. Conclusions: The findings provide preliminary support for non-replay dreams to satisfy the DSM B2 diagnostic criterion when the affect associated with those dreams is the same as that experienced at the time of the traumatic event.
National Guideline of Rabies Prophylaxis-2010
Authors: Amin Mohammad Robed 
Published: August 2011

Background: Rabies has been the subject of fear ever since the disease was recognized. Worldwide the number of deaths annually, due to rabies, is estimated to be between 35,000 to 50,000 approximately Rabies continues to be a major public health problem in Bangladesh killing an estimated 2000 people annually and 100,000 people receive post-exposure treatment in the country. In this regard the post-exposure treatment of animal bite cases is of prime importance. Materials and Methods: Communicable disease control(CDC) of, Directorate General of Health Services (DGHS) took the noble initiative to establish the national rabies elimination programme 2010 with an comprehensive approach of care for human and control of rabid animal. An expert group meeting for strategic plan and finalizing the guidelines for prevention and control of rabies cases was held in 2010, under CDC of DGHS to bring out uniformity in post-exposure treatment practices. . The participants in the meeting included practitioners managing anti-rabies clinics, laboratory medicine practitioners, policy makers, public health experts from both public and private sector. The guideline, which emerged out of consensus of expert groups, is summarized in this paper. Results: Until recently the Nervous Tissue Vaccine (NTV) was the mainstay for post-exposure prophylaxis in Bangladesh. As per WHO recommendations, the production and use of this reactogenic vaccine should be gradually phased out from our country. Modern, safe and effective anti-rabies Cell Culture Vaccines (CCVs) will be used for post-exposure prophylaxis in public sectors. The limitation is the high cost of this vaccine and also the cost and unavailability of Anti Rabies Immunoglobulin. WHO recommended the use of intra-dermal (ID) route of application of CCVs. Considering the recommendations of experts, results of clinical trials and international experience, experts of Bangladesh recommends ID regimen phase wise. In first phase, only Dhaka Infectious Disease Hospital will serve as Anti-rabies centre for ID regimen. After its successful implementation, ID regimen will spread out to Division and then to District level hospitals. National experts suggested and recommended the use of cost-effective vaccination schedules such as abbreviated multisite IM Zagreb protocol (4 dose, 3 visits) and updated Thai Red Cross (TRC) intradermal regimen(2-2-2-0-2) to phase out NTV and to make available modern rabies vaccine in public sector. Conclusion: This guideline will be extremely useful for the country to make rational use of modern rabies vaccine and phase out NTV by 2011. The guideline will be of immense use for better management of animal bite cases and availability and affordability of modern rabies vaccine will be of great help for physician to manage appropriately for preventing the deadly disease rabies. DOI: http://dx.doi.org/10.3329/jom.v12i2.7691 JOM 2011; 12(2): 153-159
The Facultative Intracellular Pathogen Candida glabrata Subverts Macrophage Cytokine Production and Phagolysosome Maturation
Authors: Seider Katja , Brunke Sascha , Schild Lydia , Jablonowski Nadja , Wilson Duncan , Majer Olivia , Barz Dagmar , Haas Albert , Kuchler Karl , Schaller Martin , Hube Bernhard 
Published: August 2011

Abstract
Although Candida glabrata is an important human pathogenic yeast, its pathogenicity mechanisms are largely unknown. Immune evasion strategies seem to play key roles during infection, since very little inflammation is observed in mouse models. Furthermore, C. glabrata multiplies intracellularly after engulfment by macrophages. In this study, we sought to identify the strategies that enable C. glabrata to survive phagosome biogenesis and antimicrobial activities within human monocyte-derived macrophages. We show that, despite significant intracellular proliferation, macrophage damage or apoptosis was not apparent, and production of reactive oxygen species was inhibited. Additionally, with the exception of GM-CSF, levels of pro- and anti-inflammatory cytokines were only marginally increased. We demonstrate that adhesion to and internalization by macrophages occur within minutes, and recruitment of endosomal early endosomal Ag 1 and lysosomal-associated membrane protein 1 indicates phagosome maturation. However, phagosomes containing viable C. glabrata, but not heat-killed yeasts, failed to recruit cathepsin D and were only weakly acidified. This inhibition of acidification did not require fungal viability, but it had a heat-sensitive surface attribute. Therefore, C. glabrata modifies the phagosome into a nonacidified environment and multiplies until the host cells finally lyse and release the fungi. Our results suggest persistence of C. glabrata within macrophages as a possible immune evasion strategy.
The Transport and Inactivation Kinetics of Bacterial Lipopolysaccharide Influence Its Immunological Potency In Vivo
Authors: Lu Mingfang , Munford Robert S. 
Published: August 2011

Abstract
The extraordinary potency and pathological relevance of Gram-negative bacterial LPSs have made them very popular experimental agonists, yet little is known about what happens to these stimulatory molecules within animal tissues. We tracked fluorescent and radiolabeled LPS from a s.c. inoculation site to its draining lymph nodes (DLN), blood, and liver. Although we found FITC-labeled LPS in DLN within minutes of injection, drainage of radiolabeled LPS continued for &gt;6 wk. Within the DLN, most of the LPS was found in the subcapsular sinus or medulla, near or within lymphatic endothelial cells and CD169+ macrophages. Whereas most of the LPS seemed to pass through the DLN without entering B cell follicles, by 24 h after injection a small amount of LPS was found in the paracortex. In wild-type mice, ≥70% of the injected radiolabeled LPS underwent inactivation by deacylation before it left the footpad; in animals that lacked acyloxyacyl hydrolase, the LPS-deacylating enzyme, prolonged drainage of fully acylated (active) LPS boosted polyclonal IgM and IgG3 Ab titers. LPS egress from a s.c. injection site thus occurred during many weeks and was mainly via lymphatic channels. Its immunological potency, as measured by its ability to stimulate polyclonal Ab production, was greatly influenced by the kinetics of both lymphatic drainage and enzymatic inactivation.
The CD6 Multiple Sclerosis Susceptibility Allele Is Associated with Alterations in CD4+ T Cell Proliferation
Authors: Kofler David M. , Severson Christopher A. , Mousissian Narine , De Jager Philip L. , Hafler David A. 
Published: August 2011

Abstract
Genome-wide association studies have revealed a large number of genetic associations with autoimmune diseases. Despite this progress, the mechanisms underlying the contribution of allelic variants to the onset of immune-related diseases remain mostly unknown. Our recent meta-analysis of genome-wide association studies of multiple sclerosis (MS) identified a new susceptibility locus tagged by a single nucleotide polymorphism, rs17824933 (p = 3.8 × 10−9), that is found in a block of linkage disequilibrium containing the CD6 gene. Because CD6 plays an important role in maintenance of T cell activation and proliferation, we examined the biologic phenotypes of the risk-associated allele. In this article, we report that the MS susceptibility allele in CD6 is associated with decreased expression of full-length CD6 in CD4+ and CD8+ T cells. As a consequence, proliferation is diminished during long-term activation of CD4+ T cells from subjects with the risk allele. Selective knockdown of full-length CD6 using exon 5-specific small interfering RNA induces a similar proliferation defect of CD4+ T cells from subjects homozygous for the protective allele. Exon 5 encodes for the extracellular binding site of the CD6 ligand ALCAM, which is required for CD6 stimulation. In CD4+ T cells from subjects with the risk allele, exon 5 is consistently underexpressed, thereby providing a mechanism by which the allele affects proliferation of CD4+ T cells. These findings indicate that the MS risk allele in the CD6 locus is associated with altered proliferation of CD4+ T cells and demonstrate the influence of a disease-related allelic variant on important immunological characteristics.
Membrane-Associated CD93 Regulates Leukocyte Migration and C1q-Hemolytic Activity during Murine Peritonitis
Authors: Greenlee-Wacker Mallary C. , Briseño Carlos , Galvan Manuel , Moriel Gabriela , Velázquez Peter , Bohlson Suzanne S. 
Published: August 2011

AbstractCD93 is emerging as a novel regulator of inflammation; however, its molecular function is unknown. CD93 exists as a membrane-associated glycoprotein on the surface of cells involved in the inflammatory cascade, including endothelial and myeloid cells. A soluble form (sCD93) is detectable in blood and is elevated with inflammation. In this study, we demonstrate heightened susceptibility to thioglycollate-induced peritonitis in CD93−/− mice. CD93−/− mice showed a 1.6–1.8-fold increase in leukocyte infiltration during thioglycollate-induced peritonitis between 3 and 24 h that returned to wild type levels by 96 h. Impaired vascular integrity in CD93−/− mice during peritonitis was demonstrated using fluorescence multiphoton intravital microscopy; however, no differences in cytokine or chemokine levels were detected with Luminex Multiplex or ELISA analysis. C1q-hemolytic activity in CD93−/− mice was decreased by 22% at time zero and by 46% 3 h after thioglycollate injection, suggesting a defect in the classical complement pathway. Leukocyte recruitment and C1q-hemolytic activity was restored to wild type levels when CD93 was expressed on either hematopoietic cells or nonhematopoietic cells in bone marrow chimeric mice. However, elevated levels of sCD93 in inflammatory fluid were observed only when CD93 was expressed on nonhematopoietic cells. Because cell-associated CD93 was sufficient to restore a normal inflammatory response, these data suggest that cell-associated CD93, and not sCD93, regulates leukocyte recruitment and complement activation during murine peritonitis.
IL-10 Restricts Activation-Induced Death of NK Cells during Acute Murine Cytomegalovirus Infection
Authors: Stacey Maria A. , Marsden Morgan , Wang Eddie C. Y. , Wilkinson Gavin W. G. , Humphreys Ian R. 
Published: August 2011

Abstract
IL-10 is an immunomodulatory cytokine that acts to antagonize T cell responses elicited during acute and chronic infections. Thus, the IL-10R signaling pathway provides a potential therapeutic target in strategies aimed at combating infectious diseases. In this study, we set out to investigate whether IL-10 expression had an effect on NK cells. Murine CMV infection provides the best characterized in vivo system to evaluate the NK cell response, with NK cells being critical in the early control of acute infection. Blockade of IL-10R during acute murine CMV infection markedly reduced the accumulation of cytotoxic NK cells in the spleen and lung, a phenotype associated with a transient elevation of virus DNA load. Impaired NK cell responsiveness after IL-10R blockade was attributed to elevated levels of apoptosis observed in NK cells exhibiting an activated phenotype. Therefore, we conclude that IL-10 contributes to antiviral innate immunity during acute infection by restricting activation-induced death in NK cells.
MicroRNA-21 Limits In Vivo Immune Response-Mediated Activation of the IL-12/IFN-γ Pathway, Th1 Polarization, and the Severity of Delayed-Type Hypersensitivity
Authors: Lu Thomas X. , Hartner Jochen , Lim Eun-Jin , Fabry Victoria , Mingler Melissa K. , Cole Eric T. , Orkin Stuart H. , Aronow Bruce J. , Rothenberg Marc E. 
Published: August 2011

Abstract
An altered balance between Th1 and Th2 cytokines is responsible for a variety of immunoinflammatory disorders such as asthma, yet the role of posttranscriptional mechanisms, such as those mediated by microRNAs (miRs), in adjusting the relative magnitude and balance of Th cytokine expression have been largely unexplored. In this study, we show that miR-21 has a central role in setting a balance between Th1 and Th2 responses to Ags. Targeted ablation of miR-21 in mice led to reduced lung eosinophilia after allergen challenge, with a broadly reprogrammed immunoactivation transcriptome and significantly increased levels of the Th1 cytokine IFN-γ. Biological network-based transcriptome analysis of OVA-challenged miR-21−/− mice identified an unexpected prominent dysregulation of IL-12/IFN-γ pathways as the most significantly affected in the lungs, with a key role for miR-21 in IFN-γ signaling and T cell polarization, consistent with a functional miR-21 binding site in IL-12p35. In support of these hypotheses, miR-21 deficiency led dendritic cells to produce more IL-12 after LPS stimulation and OVA-challenged CD4+ T lymphocytes to produce increased IFN-γ and decreased IL-4. Further, loss of miR-21 significantly enhanced the Th1-associated delayed-type hypersensitivity cutaneous responses. Thus, our results define miR-21 as a major regulator of Th1 versus Th2 responses, defining a new mechanism for regulating polarized immunoinflammatory responses.
Recognition and Killing of Human and Murine Pancreatic β Cells by the NK Receptor NKp46
Authors: Gur Chamutal , Enk Jonatan , Kassem Sameer A. , Suissa Yaron , Magenheim Judith , Stolovich-Rain Miri , Nir Tomer , Achdout Hagit , Glaser Benjamin , Shapiro James , Naparstek Yaakov , Porgador Angel , Dor Yuval , Mandelboim Ofer 
Published: August 2011

Abstract
Type 1 diabetes is an incurable disease that is currently treated by insulin injections or in rare cases by islet transplantation. We have recently shown that NKp46, a major killer receptor expressed by NK cells, recognizes an unknown ligand expressed by β cells and that in the absence of NKp46, or when its activity is blocked, diabetes development is inhibited. In this study, we investigate whether NKp46 is involved in the killing of human β cells that are intended to be used for transplantation, and we also thoroughly characterize the interaction between NKp46 and its human and mouse β cell ligands. We show that human β cells express an unknown ligand for NKp46 and are killed in an NKp46-dependent manner. We further demonstrate that the expression of the NKp46 ligand is detected on human β cells already at the embryonic stage and that it appears on murine β cells only following birth. Because the NKp46 ligand is detected on healthy β cells, we wondered why type 1 diabetes does not develop in all individuals and show that NK cells are absent from the vicinity of islets of healthy mice and are detected in situ in proximity with β cells in NOD mice. We also investigate the molecular mechanisms controlling NKp46 interactions with its β cell ligand and demonstrate that the recognition is confined to the membrane proximal domain and stalk region of NKp46 and that two glycosylated residues of NKp46, Thr125 and Asn216, are critical for this recognition.
Hierarchical IL-5 Expression Defines a Subpopulation of Highly Differentiated Human Th2 Cells
Authors: Upadhyaya Bhaskar , Yin Yuzhi , Hill Brenna J. , Douek Daniel C. , Prussin Calman 
Published: August 2011

Abstract
Each of the three Th2 cytokine genes, IL-4, IL-5, and IL-13, has different functions. We hypothesized that Th2 heterogeneity could yield Th2 subpopulations with different cytokine expression and effector functions. Using multiple approaches, we demonstrate that human Th2 cells are composed of two major subpopulations: a minority IL-5+ (IL-5+, IL-4+, IL-13+) and majority IL-5− Th2 (IL-5−, IL-4+, IL-13+) population. IL-5+ Th2 cells comprised only 20% of all Th2 cells. Serial rounds of in vitro differentiation initially yielded IL-5− Th2, but required multiple rounds of differentiation to generate IL-5+ Th2 cells. IL-5+ Th2 cells expressed less CD27 and greater programmed cell death-1 than IL-5− Th2 cells, consistent with their being more highly differentiated, Ag-exposed memory cells. IL-5+ Th2 cells expressed greater IL-4, IL-13, and GATA-3 relative to IL-5− Th2 cells. GATA-3 and H3K4me3 binding to the IL5 promoter (IL5p) was greater in IL-5+ relative to IL-5− Th2 cells, whereas there was no difference in their binding to the IL4p and IL13p. Conversely, H3K27me3 binding to the IL5p was greater in IL-5− Th2 cells. These findings demonstrate Th2 lineage heterogeneity, in which the IL5 gene is regulated in a hierarchical manner relative to other Th2 genes. IL-5+ Th2 cells are phenotypically distinct and have epigenetic changes consistent with greater IL5p accessibility. Recurrent antigenic exposure preferentially drives the differentiation of IL-5+ Th2 cells. These results demonstrate that IL-5+ and IL-5− Th2 cells, respectively, represent more and less highly differentiated Th2 cell subpopulations. Such Th2 subpopulations may differentially contribute to Th2-driven pathology.
Caveolin-1 Orchestrates TCR Synaptic Polarity, Signal Specificity, and Function in CD8 T Cells
Authors: Tomassian Tamar , Humphries Lisa A. , Liu Scot D. , Silva Oscar , Brooks David G. , Miceli M. Carrie 
Published: August 2011

Abstract
TCR engagement triggers the polarized recruitment of membrane, actin, and transducer assemblies within the T cell–APC contact that amplify and specify signaling cascades and T effector activity. We report that caveolin-1, a scaffold that regulates polarity and signaling in nonlymphoid cells, is required for optimal TCR-induced actin polymerization, synaptic membrane raft polarity, and function in CD8, but not CD4, T cells. In CD8+ T cells, caveolin-1 ablation selectively impaired TCR-induced NFAT-dependent NFATc1 and cytokine gene expression, whereas caveolin-1 re-expression promoted NFATc1 gene expression. Alternatively, caveolin-1 ablation did not affect TCR-induced NF-κB–dependent Iκbα expression. Cav-1−/− mice did not efficiently promote CD8 immunity to lymphocytic choriomeningitis virus, nor did cav-1−/− OT-1+ CD8+ T cells efficiently respond to Listeria monocytogenes-OVA after transfer into wild-type hosts. Therefore, caveolin-1 is a T cell-intrinsic orchestrator of TCR-mediated membrane polarity and signal specificity selectively employed by CD8 T cells to customize TCR responsiveness.
Ubiquitination of CD86 Is a Key Mechanism in Regulating Antigen Presentation by Dendritic Cells
Authors: Baravalle Günther , Park Hyesuk , McSweeney Megan , Ohmura-Hoshino Mari , Matsuki Yohei , Ishido Satoshi , Shin Jeoung-Sook 
Published: August 2011

Abstract
Dendritic cells (DCs) require costimulatory molecules such as CD86 to efficiently activate T cells for the induction of adaptive immunity. DCs maintain minimal levels of CD86 expression at rest, but upregulate levels upon LPS stimulation. LPS-stimulated DCs produce the immune suppressive cytokine IL-10 that acts in an autocrine manner to regulate CD86 levels. Interestingly, the underlying molecular mechanism behind the tight control of CD86 is not completely understood. In this study, we report that CD86 is ubiquitinated in DCs via MARCH1 E3 ubiquitin ligase and that this ubiquitination plays a key role in CD86 regulation. Ubiquitination at lysine 267 played the most critical role for this regulation. CD86 is ubiquitinated in MARCH1-deficient DCs to a much lesser degree than in wild-type DCs, which also correlated with a significant increase in CD86 expression. Importantly, CD86 is continuously ubiquitinated in DCs following activation by LPS, and this was due to the autocrine IL-10 inhibition of MARCH1 downregulation. Accordingly, DCs lacking MARCH1 and DCs expressing ubiquitination-resistant mutant CD86 both failed to regulate CD86 in response to autocrine IL-10. DCs expressing ubiquitination-resistant mutant CD86 failed to control their T cell-activating abilities at rest as well as in response to autocrine IL-10. These studies suggest that ubiquitination serves as an important mechanism by which DCs control CD86 expression and regulate their Ag-presenting functions.
Regulatory T Cells Selectively Control CD8+ T Cell Effector Pool Size via IL-2 Restriction
Authors: Kastenmuller Wolfgang , Gasteiger Georg , Subramanian Naeha , Sparwasser Tim , Busch Dirk H. , Belkaid Yasmine , Drexler Ingo , Germain Ronald N. 
Published: August 2011

Abstract
Regulatory T cells (Treg) are key players in maintaining immune homeostasis but have also been shown to regulate immune responses against infectious pathogens. Therefore, Treg are a promising target for modulating immune responses to vaccines to improve their efficacy. Using a viral vector system, we found that Treg act on the developing immune response early postinfection by reducing the extent of dendritic cell costimulatory molecule expression. Due to this change and the lower IL-2 production that results, a substantial fraction of CD8+ effector T cells lose CD25 expression several days after activation. Surprisingly, such Treg-dependent limitations in IL-2 signaling by Ag-activated CD8+ T cells prevent effector differentiation without interfering with memory cell formation. In this way, Treg fine-tune the numbers of effector T cells generated while preserving the capacity for a rapid recall response upon pathogen re-exposure. This selective effect of Treg on a subpopulation of CD8+ T cells indicates that although manipulation of the Treg compartment might not be optimal for prophylactic vaccinations, it can be potentially exploited to optimize vaccine efficacy for therapeutic interventions.
The evaluation of upper leg traction in lateral position for pediatric caudal block
Authors: Seyedhejazi Mahin , Taheri Reza , Ghojazadeh Morteza 
Published: August 2011

Purpose:
A well-functioning caudal block is an excellent adjunct to general anesthesia, but misplaced injection results in poor analgesia as well as possibility of serious morbidity. Therefore, the purpose of this study was to evaluate the effectiveness of leg traction on success rate of caudal block in lateral position in children.

Methods:
Two hundred children, age 2 months to 6 years, ASA I and II, who underwent lower abdominal surgeries were randomized in prospective controlled clinical trial study in two groups. After induction of General anesthesia, the caudal block was performed in the lateral position with upper leg traction (L-T-) or with the standard position (S-P) (leg flexed 90°). Hemodynamicchanges, movement of lower extremity in response to surgical stimulus were evaluated.

Results:
There was no significant difference in caudal block's success rate between two groups at first attempt (P=0.25). In group (S-P) the procedure was successful in 60% of cases at first attempt, 25% at second,10% at third attempt and 5% failure of caudal block, whereas in the first group it was 75%, 20%, 1% and 4% of cases respectively. There were no significant differences in heart rate and blood pressure changes between two groups (P>0.05).

Conclusion:
The success rate of pediatric caudal block in upper leg traction did not differ from that of the standard position.