bluuebunny/crossref_metadata_2025_split huggingface dataset:
Posttraumatic stress disorder and psychiatric co-morbidity: symptoms in a random sample of female Bosnian refugees
Authors: Sundquist Kristina , Johansson Leena-Maria , DeMarinis Valeri , Johansson Sven-Erik , Sundquist Jan 
Published: February 2005

AbstractObjectivesThis study investigated psychological symptoms in Bosnian women 3–4 years after their arrival in Sweden.MethodsA simple random sample of 163 Bosnian women aged 19–59 was drawn from the Swedish populations register in 1996. The control group consisted of 392 Swedish-born women. Data were collected in face-to-face interviews. The Hopkins Symptom Checklist 25 (HSCL-25) and the Posttraumatic Symptom Scale (PTSS-10) were used to measure psychological symptoms of depression, anxiety, psychological distress, and posttraumatic stress disorder (PTSD). Unconditional logistic regression was used to estimate odds ratios (OR) for psychological symptoms after adjustment for age, country of birth, education, marital status, economic difficulties, social network, and feeling secure.ResultsThe prevalence of symptoms of PTSD was 28.3% among the Bosnian women. Bosnian women had significantly higher risks of symptoms of depression, anxiety, and psychological distress than Swedish-born women. For depression the odds ratio was 9.50 among Bosnian women.ConclusionsPsychiatric community interventions need to target Bosnian refugee women. Awareness among health-care workers who encounter these women in a clinical setting should be improved.
Histopathology of carotid body in heroin addiction. Possible chemosensitive impairment
Authors: Porzionato A , Macchi V , Guidolin D , Parenti A , Ferrara S D , De Caro R 
Published: February 2005

Aims : To perform a morphometric analysis of carotid bodies in opiate addicts.Methods and results : Carotid bodies were sampled at autopsy from 35 subjects who died of heroin intoxication (mean age 26 years), and from eight young (22 years) and eight older subjects (66.5 years) who died of trauma. Sections were stained with haematoxylin–eosin, azan‐Mallory, and double‐labelling immunohistochemistry with antineuronal specific enolase and anti‐S100, to count type I and type II cells. Interlobular and intralobular connective tissue was increased both in the opiate cases (43.45 ± 6.79%, P < 0.001, and 13.34 ± 5.72%, P < 0.001, respectively) and older cases (46.67 ± 1.65%, P < 0.001, and 9.62 ± 2.11%, P < 0.05, respectively) compared with young cases (33.17 ± 6.41% and 4.33 ± 1.84%, respectively). The percentage of type II cells in the opiate cases (51.6 ± 7.3%, P < 0.001) and in the older controls (49.0 ± 7.2%, P < 0.01) was higher than in the young cases (37.9 ± 3.0%). Among type I cells, the light cell percentage in the opiate cases (65.85 ± 11%, P < 0.001) was reduced with respect to the two control groups (82.8 ± 5.34%, young; 81.62 ± 8.58%, older).Conclusions : The increases in connective tissue and type II cells are similar to findings in ageing and chronic pulmonary disease, and may be ascribed to glomic hypoxia. A direct action of opiates should be taken into account for the decrease in light cells in heroin addiction. The histopathological changes in the carotid body, by impairing chemosensivity, may play a role in the fatal cardiorespiratory derangement of heroin addicts.
The distribution of cardiac macrophages in myocardial ischaemia and cardiomyopathy
Authors: Azzawi M , Kan S W , Hillier V , Yonan N , Hutchinson I V , Hasleton P S 
Published: February 2005

Aims : Recent evidence has implicated the macrophage as an effector cell in the inflammatory processes in transplant rejection, as well as cardiac disease, including coronary atherosclerosis. Although the latter is a vascular disease, the entire myocardium is affected. We have previously demonstrated the presence and distribution of macrophages in the ‘normal’ human heart. In this paper the distribution of myocardial macrophages, in the various chambers of the failing human heart, from cases of coronary atheroma and cardiomyopathy undergoing heart transplantation is documented.Methods and results : Tissue blocks were removed at specific sites taken from six cases with ischaemic heart disease (IHD) (four males, two females, age range 54–62 years), and four cases with idiopathic dilated cardiomyopathy (IDCM) (three males, one female, age range 18–49 years). These were compared with hearts from five cases of sudden death, unrelated to heart disease. Sections were stained with a CD68 pan macrophage marker. Positive cells were enumerated in 20 random fields. Results were analysed using a generalized linear modelling method using a Poisson distribution. Macrophages were identified within the interstitium and often close to blood vessels in all hearts. Macrophages from IHD hearts demonstrated the most intense staining and were often larger and more elongated than those found in ‘normal’ control hearts. Macrophages were also often degranulated and staining was diffuse in the interstitium. Overall, there were significantly more macrophages in most areas from IHD hearts than from IDCM hearts or control hearts (P < 0.001).Conclusions : Significantly more macrophages were found in all four chambers in diseased hearts compared with controls. Macrophage numbers were higher in the atria than in ventricles in the diseased myocardium. This study suggests selective recruitment of macrophages into the atria in the disease states studied.
Retroviral Foxp3 gene transfer ameliorates liver granuloma pathology in Schistosoma mansoni infected mice
Authors: Singh Kameshwar P. , Gerard Herve C. , Hudson Alan P. , Reddy Thipparthi R. , Boros Dov L. 
Published: February 2005

SummarySchistosomiasis mansoni, a tropical helminthic disease, is caused by disseminated worm eggs that induce CD4+ T‐cell mediated granulomatous inflammation and fibrosis. T suppressor cell activity has been proposed as one of the mechanisms active in the down‐modulation of the murine disease during the chronic stage (16–20 weeks of the infection). In recent years a new category of the CD4+ CD25+ T regulatory (Treg) lymphocyte has been identified that maintains immune tolerance to self, and also functions in the regulation of parasite‐induced immunopathology. The Foxp3 gene which encodes the transcription factor Scurfin was found to be expressed by and required for the generation of CD4+ CD25+ T reg. At 8 weeks of the infection Foxp3 gene expression of splenocytes was similar to that of naïve mice, but increased fourfold by 16 weeks. In contrast, granulomatous livers at 8 and 16 weeks showed 10‐ and 30‐fold increases, respectively, in gene expression compared with normal liver. The percentage of granuloma CD4+ CD25+ T cells rose from 12% at 8 weeks to 88% at 16 weeks of the infection. Foxp3 expression was 3·5‐fold higher in the CD4+ CD25+ versus the CD4+ CD25– T cells in the 8 week infection granulomas. As a novel observation neuropilin‐1 membrane expression, a recently identified marker for Treg, was correlated with Foxp3 expression in the granuloma CD4+ CD25+ but not the CD25– cells. Co‐incubation with polyclonal stimulation of CD4+ CD25+ splenic cells with CD4+ CD25– cells suppressed proliferation of the latter. Retroviral transfer of the Foxp3 gene at the onset of granuloma formation enhanced fourfold Foxp3 expression in the granuloma CD4+ CD25+ T cells and strongly suppressed full granuloma development. Gene transfer also significantly enhanced transforming growth factor‐β, interferon‐γ and interleukin‐4 but not interleukin‐10 expression. It is concluded, that CD4+ CD25+, Foxp3+ Treg cells also regulate schistosome egg‐induced immunopathology.
Interleukin‐7 signalling is sufficient to phenotypically and functionally prime human CD4+ naïve T cells
Authors: Managlia Elizabeth Z. , Landay Alan , Al‐Harthi Lena 
Published: February 2005

SummaryInterleukin‐7 (IL‐7) is produced by bone marrow and lymphoid stromal cells and is involved in the synthesis, survival and homeostasis of T cells. These attributes are the basis for current strategies to utilize IL‐7 as an immune modulator for several clinical conditions to replenish depleted T‐cell numbers. Because we had previously determined that IL‐7 can induce potent human immunodeficiency virus replication in the otherwise non‐permissive CD4+ naïve T‐cell compartment, we evaluated here the impact of IL‐7 on the phenotype and functional potential of naïve CD4+ T cells in an attempt to understand the mechanism of this induction. We demonstrate that IL‐7 mediated the up‐regulation of CD25, CD95 and human leucocyte antigen‐DR, while it did not alter the expression of CD45RO, CD69, CD40, or CD154. Examination of the cytokine profile of IL‐7‐treated naïve T cells using a Type1/Type2 Proteome Array indicated a remarkable IL‐7‐mediated induction of interferon‐γ production, while the other cytokines evaluated (IL‐2, IL‐12, tumour necrosis factor‐α, IL‐4, IL‐5, IL‐10 and IL‐13) were not affected. Intracellular staining of IL‐7‐treated naïve T cells for interferon‐γ verified the Proteome data. IL‐7 did not induce cell cycle proliferation of naïve CD4+ T cells, as evaluated by 7‐AAD/pyronin immunostaining and carboxyfluorescein diacetate succinimidyl ester dye tracking. IL‐7 treatment of naïve CD4+ T cells induced their ability to prime monocytes, as was indicated by induction of CD80 and CD86 expression on monocytes cocultured with IL‐7‐treated naïve CD4+ T cells. Collectively, these data indicate that IL‐7 signalling is sufficient to phenotypically and functionally prime human CD4+ naïve T cells independent of antigen stimulation.
Cross‐linking of neutrophil CD11b results in rapid cell surface expression of molecules required for antigen presentation and T‐cell activation
Authors: Sandilands Gavin P. , Ahmed Zubir , Perry Nicole , Davison Martin , Lupton Alison , Young Barbara 
Published: February 2005

SummaryRecent studies suggest that neutrophils may play a role in antigen presentation. In support of this hypothesis it has been shown that these cells appear to contain cytoplasmic stores of molecules required for this function, i.e. major histocompatibility complex class II (DR) antigen, CD80 and CD86. In this study we have considered a mechanism for the translocation of these preformed molecules onto the cell surface which does not require active synthesis. Cross‐linking of the Mac‐1 molecule (CD18 + CD11b) was shown to result in rapid cell surface expression of CD80, CD86 and DR antigen on the surface of normal human peripheral blood neutrophils. A distinct subpopulation (approximately 20%) of neutrophils appeared to be enlarged and were found to express significantly elevated levels of these molecules on the cell surface following cross‐linking of CD11b when compared with control cells. The level of expression of CD80, CD86 and DR antigen on these large cells was comparable to, and in some cases greater than, the levels found expressed on the surface of monocytes obtained from the same donors. In addition, these cytoplasmic molecules were shown by confocal laser microscopy and by immunoelectron microscopy to be located within secretory vesicles. Following rapid translocation onto the cell surface, CD80 and CD86 appeared to be colocalized within large clusters reminiscent of the supramolecular antigen clusters previously found on conventional antigen‐presenting cells. These findings therefore lend further support for the hypothesis that neutrophils may have a role to play in antigen presentation and/or T‐cell activation.
Stoichiometric tapasin interactions in the catalysis of major histocompatibility complex class I molecule assembly
Authors: Bangia Naveen , Cresswell Peter 
Published: February 2005

SummaryThe assembly of major histocompatibility complex (MHC) class I molecules with their peptide ligands in the endoplasmic reticulum (ER) requires the assistance of many proteins that form a multimolecular assemblage termed the ‘peptide‐loading complex’. Tapasin is the central stabilizer of this complex, which also includes the transporter associated with antigen processing (TAP), MHC class I molecules, the ER chaperone, calreticulin, and the thiol‐oxidoreductase ERp57. In the present report, we investigated the requirements of these interactions for tapasin protein stability and MHC class I dissociation from the peptide‐loading complex. We established that tapasin is stable in the absence of either TAP or MHC class I interaction. In the absence of TAP, tapasin interaction with MHC class I molecules is long‐lived and results in the sequestration of existing tapasin molecules. In contrast, in TAP‐sufficient cells, tapasin is re‐utilized to interact with and facilitate the assembly of many MHC class I molecules sequentially. Furthermore, chemical cross‐linking has been utilized to characterize the interactions within this complex. We demonstrate that tapasin and MHC class I molecules exist in a 1 : 1 complex without evidence of higher‐order tapasin multimers. Together these studies shed light on the tapasin protein life cycle and how it functions in MHC class I assembly with peptide for presentation to CD8+ T cells.
Migration of polymorphonuclear leucocytes is influenced by dendritic cells
Authors: Scimone M. Lucila , Lutzky Viviana P. , Zittermann Sandra I. , Maffia Paulo , Jancic Carolina , Buzzola Fernanda , Issekutz Andrew C. , Chuluyan H. Eduardo 
Published: February 2005

SummaryDendritic cells (DCs) are the most potent antigen‐presenting cells and populate many tissues where they may participate in inflammatory reactions. The infiltration of polymorphonuclear leucocytes (PMNLs) into tissues is a prominent feature of inflammation. The mechanisms of PMNL recruitment depend on chemotactic factors and adhesion molecules expressed on endothelial cells. The aim of the present study was to determine whether DCs participate in the early recruitment of PMNLs. Dendritic cells derived from peripheral blood monocytes were used for this study. PMNLs incubated with culture supernatant (CS) from untreated or from tumour necrosis factor‐α (TNF‐α)‐treated (1 hr, 100 U/ml, 37°) monocyte‐derived DCs (moDCs) had increased surface expression of both CD11b and CD18. Moreover, both untreated and TNF‐α‐treated moDCs induced PMNL chemotaxis. By blocking CXCL8, CXCL5, CXCL7 and Pan GRO (CXCL1, CXCL2, CXCL3), we observed that CXCL8/interleukin‐8 might be the chemokine that induced the PMNL chemotactic activity in the CS of untreated and TNF‐α‐treated moDC. Furthermore, we investigated the regulation of CXCL8 production in moDCs by adhesion molecule engagement. Our data demonstrated that CD31, CD18, CD29 and CD49d participated in the adhesion of immature moDCs to endothelium. Moreover, engagement of domains 1–3 of CD31, but not of CD29 or CD18, decreased the production of CXCL8 by immature but not mature moDCs (which display lower CD31 levels than immature moDCs). Overall, these results suggest that DCs not only trigger a specific immune response, but also the innate immune response by recruiting PMNLs. Furthermore, our results also suggest that CXCL8 production by immature DCs might be regulated by signalling through CD31 during their migration through the vascular endothelium.
Interleukin‐10 (IL‐10) mediated suppression of IL‐12 production in RAW 264.7 cells also involves c‐rel transcription factor
Authors: Rahim Sheikh Showkat , Khan Nooruddin , Boddupalli Chandra Sekhar , Hasnain Seyed E. , Mukhopadhyay Sangita 
Published: February 2005

SummaryInterleukin‐10 (IL‐10) is known to inhibit IL‐12 production in macrophages primarily at the transcriptional level with the involvement of p50 and p65 nuclear factor‐κB (NF‐κB). We demonstrate that the c‐rel transcription factor also plays a major role in IL‐10‐mediated IL‐12 suppression. Treatment of macrophages with recombinant IL‐10 inhibited nuclear c‐rel levels, whereas addition of neutralizing anti‐IL‐10 antibody up‐regulated both nuclear c‐rel levels and IL‐12 production by macrophages. Decreased nuclear c‐rel was associated with a reduction in phosphorylation of inhibitory kappa B alpha (IκBα) in the cytoplasm, indicating that IL‐10 prevents degradation of IκBα and the subsequent translocation of c‐rel into the nucleus. Treatment with leptomycin B, a known inhibitor of c‐rel at a concentration of 10 nm, when used with anti‐IL‐10 antibody, resulted in reduced expression of IL‐12. In a complementary experiment, in vitro transient expression of p65 NF‐κB could not rescue the inhibitory effect of IL‐10 on IL‐12 production, suggesting that NF‐κB alone was not sufficient to restore IL‐12 production during IL‐10 treatment. However, over‐expression of c‐rel resulted in IL‐12 restoration upon stimulation with lipopolysaccharide plus interferon‐γ during IL‐10 treatment. Our studies highlight the involvement of c‐rel in IL‐10‐mediated IL‐12 regulation.
Evolution of a phage RuvC endonuclease for resolution of both Holliday and branched DNA junctions
Authors: Curtis Fiona A. , Reed Patricia , Sharples Gary J. 
Published: February 2005

SummaryResolution of Holliday junction recombination intermediates in most Gram‐negative bacteria is accomplished by the RuvC endonuclease acting in concert with the RuvAB branch migration machinery. Gram‐positive species, however, lack RuvC, with the exception of distantly related orthologues from bacteriophages infecting Lactococci and Streptococci. We have purified one of these proteins, 67RuvC, from Lactococcus lactis phage bIL67 and demonstrated that it functions as a Holliday structure resolvase. Differences in the sequence selectivity of resolution between 67RuvC and Escherichia coli RuvC were noted, although both enzymes prefer to cleave 3′ of thymidine residues. However, unlike its cellular counterpart, 67RuvC readily binds and cleaves a variety of branched DNA substrates in addition to Holliday junctions. Plasmids expressing 67RuvC induce chromosomal breaks, probably as a consequence of replication fork cleavage, and cannot be recovered from recombination‐defective E. coli strains. Despite these deleterious effects, 67RuvC constructs suppress the UV light sensitivity of ruvA, ruvAB and ruvABC mutant strains confirming that the phage protein mediates Holliday junction resolution in vivo. The characterization of 67RuvC offers a unique insight into how a Holliday junction‐specific resolvase can evolve into a debranching endonuclease tailored to the requirements of phage recombination.
Delineation and characterization of the actin nucleation and effector translocation activities of Salmonella SipC
Authors: Chang JiHoon , Chen Jue , Zhou Daoguo 
Published: February 2005

Summary Salmonella type III secreted SipC possesses dual functions: translocation of effectors and actin modulation. The biological significance of SipC's actin nucleation activity in Salmonella‐induced actin cytoskeleton rearrangements has not been studied. We report here the delineation of the actin nucleation activity from the effector translocation activity of SipC. Our data show that the central amino acid region (residues: 201–220) is essential for its actin nucleation activity and the C‐terminal amino acid region (321–409) is required for translocation of effectors. A SipC nucleation‐deficient mutant, which maintained its effector translocation activity, was obtained. This nucleation‐deficient mutant had significantly reduced ability to induce actin cytoskeleton rearrangements, resulting in lower bacterial invasion into HeLa cells. Contrary to a previous report, we found that the purified recombinant wild‐type SipC199‐409 protein is monomeric in solution by size exclusion chromatography coupled with multiangle laser light scattering assays (SEC‐LS). Our data established that the actin nucleation activity of SipC plays a vital role in Salmonella‐induced membrane ruffles and subsequent bacteria invasion.
The Ras and Rho GTPases genetically interact to co‐ordinately regulate cell polarity during development in Penicillium marneffei
Authors: Boyce Kylie J. , Hynes Michael J. , Andrianopoulos Alex 
Published: February 2005

SummaryRas and Rho GTPases have been examined in a wide variety of eukaryotes and play varied and often overlapping roles in cell polarization and development. Studies in Saccharomyces cerevisiae and mammalian cells have defined some of the central activities of these GTPases. However, these paradigms do not explain the role of these proteins in all eukaryotes. Unlike yeast, but like more complex eukaryotes, filamentous fungi have Rac‐like proteins in addition to Ras and Cdc42. To investigate the unique functions of these proteins and determine how they interact to co‐ordinately regulate morphogenesis during growth and development we undertook a genetic analysis of GTPase function by generating double mutants of the Rho GTPases cflA and cflB and the newly isolated Ras GTPase rasA from the dimorphic pathogenic fungus, Penicillium marneffei. P. marneffei growth at 25°C is as multinucleate, septate, branched hyphae which are capable of undergoing asexual development (conidiation), while at 37°C, uninucleate pathogenic yeast cells which divide by fission are produced. Here we show that RasA (Ras) acts upstream of CflA (Cdc42) to regulate germination of spores and polarized growth of both hyphal and yeast cells, while also exhibiting CflA‐independent activities. CflA (Cdc42) and CflB (Rac) co‐ordinately control hyphal cell polarization despite also having unique roles in regulating conidial germination and polarized growth of yeast cells (CflA) and polarized growth of conidiophore cell types and hyphal branching (CflB).
A che‐like signal transduction cascade involved in controlling flagella biosynthesis in Rhodospirillum centenum
Authors: Berleman James E. , Bauer Carl E. 
Published: February 2005

Summary Rhodospirillum centenum is a photosynthetic bacterium capable of undergoing swim cell to swarm cell differentiation that allows this species to be motile on both liquid and solid media. Previous experiments have demonstrated that the che1 operon is required for the control of chemotactic and phototactic behaviour of both swim and swarm cells. In this report, we analyse the function of a second che‐like gene cluster in R. centenum, the che2 gene cluster. In‐frame deletion mutants of cheW2, cheB2, cheR2, cheY2, and of the entire che2 operon, exhibit defects in swim and swarm cell motility. Analysis of these strains demonstrates that they are non‐motile, and that the non‐motile phenotype is resulting from reduced polar and lateral flagella synthesis. Additionally, mutations in mcp2, ORF204, cheA2 and ORF74 remain chemotacticly and phototacticly competent at both high and low growth temperatures. Mutations in these che2 genes result in elevated levels of flagellin proteins giving rise to a hyperflagellate phenotype. We propose a model in which R. centenum utilizes a che‐like signal transduction pathway (che2) for regulating flagellum synthesis in order to optimize swim cell‐swarm cell differentiation in response to changing environmental conditions.