bluuebunny/crossref_metadata_2025_split huggingface dataset:
Breakdown of teenage placements in Swedish foster and residential care
Authors: Sallnäs Marie , Vinnerljung Bo , Kyhle Westermark Pia 
Published: March 2004

ABSTRACTThis article deals with the problem of breakdown in different types of out‐of‐home care (foster care/residential care) for Swedish teenagers. How often are such placements prematurely terminated against the wishes and intentions of child welfare authorities? Which factors appear to increase or decrease the risk of placement breakdown? The sample consists of a national cohort of 776 youths who started 922 placements during 1991. Every placement was followed in municipal case files for a maximum period of five years. Between 30 and 37% of all placements were prematurely terminated, the exact figure depending on whether a narrow or wide definition of breakdown was applied. The lowest rates of breakdown were found in kinship care and secure units, the highest in non‐kinship foster homes. Teenagers who display antisocial behaviour and/or have mental health problems constitute a high‐risk category for most types of out‐of‐home care, but especially in non‐kinship foster homes. Risk factors in relation to breakdown were analysed in the four main forms of Swedish out‐of‐home care separately (foster homes, privately/publicly run residential care and secure units). The analysis pointed out that risk factors are not the same in all types of care, but antisocial behaviour at time of placement increased the risk in most forms of care.Prior research indicates that placement breakdown is a major problem of child welfare in other countries, and this study found that Sweden is no exception.
The unheard client: Assessing the satisfaction of parents of children in foster care
Authors: Kapp Stephen A. , Vela Rebecca H. 
Published: March 2004

ABSTRACTAlthough client satisfaction information is often ignored, it is a critical piece of the picture when evaluating the service experience of parents who have had their children placed in foster care. This article describes the development of a client satisfaction instrument and information generated from its use. The findings describe the psychometrics of the instrument, a descriptive profile of the satisfaction scores of the respondents, and some intriguing relationships between distinct aspects of client satisfaction. The service implications of these findings are considered and discussed.
Co‐operative parenting post‐divorce: possibility or pipedream?
Authors: Walker Janet 
Published: March 2004

Research shows that, after divorce, children do best when they retain a constructive relationship with both parents. Hence, mediation services and recent reforms in family law seek to encourage parents to co‐operate fully and amicably, and to share parental responsibility for the care and well‐being of their children. There is a danger that a vision of ‘happy‐ever‐after’ post‐divorce families ignores the complexity of transitions facing separating families, and the emotional, social and economic stresses which parents experience for many years.Drawing on years of research with divorcing families, this paper invites practitioners to consider whether too much is expected of divorced parents, and whether existing services for separating families adequately address the needs of different family members.
Effect ofEscherichia coliandLactobacillus rhamnosuson Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture
Authors: Crane-Godreau Mardi A. , Wira Charles R. 
Published: March 2004

ABSTRACTEntry of bacteria from the vagina into the uterus raises the question of uterine epithelial cell (UEC) signaling in response to the presence of bacteria. Our model system helps to define microbially elicited UEC basolateral cytokine release, important in regulating underlying stromal immune cell protection. UECs from adult rats were grown in cell culture inserts to establish a confluent polarized monolayer as was determined by transepithelial resistance (TER). Polarized epithelial cell cultures were treated apically with live or heat-killedEscherichia coliorLactobacillus rhamnosusprior to collection of basolateral media after 24 h of incubation. Coculture of polarized UECs with liveE. colihad no effect on epithelial cell TER. In response to exposure to liveE. coli, epithelial cell basolateral release of macrophage inflammatory protein 3α (MIP3α) and tumor necrosis factor alpha (TNF-α) increased at a time when basolateral release of biologically active transforming growth factor β (TGF-β) decreased. Incubation of UECs with heat-killedE. coliresulted in an increased basolateral release of MIP3α and TNF-α, without affecting TER or TGF-β. In contrast toE. coli, live or heat-killedL. rhamnosushad no effect on TER or cytokine release. These studies indicate that polarized rat UECs respond to gram-negativeE. coliby releasing the cytokines MIP3α and TNF-α, signals important to both the innate and adaptive immune systems. These findings suggest that UEC responses to bacteria are selective and important in initiating and regulating immune protection in the female reproductive tract.
Toll-Like Receptor 4 Contributes to Efficient Control of Infection with the Protozoan ParasiteLeishmania major
Authors: Kropf Pascale , Freudenberg Marina A. , Modolell Manuel , Price Helen P. , Herath Shanti , Antoniazi Simone , Galanos Chris , Smith Deborah F. , Müller Ingrid 
Published: March 2004

ABSTRACTThe essential role of Toll-like receptors (TLR) in innate immune responses to bacterial pathogens is increasingly recognized, but very little is known about the role of TLRs in host defense against infections with eukaryotic pathogens. For the present study, we investigated whether TLRs contribute to the innate and acquired immune response to infection with the intracellular protozoan parasiteLeishmania major. Our results show that TLR4 contributes to the control of parasite growth in both phases of the immune response. We also addressed the mechanism that results in killing or growth of the intracellular parasites. Control of parasite replication correlates with the early induction of inducible nitric oxide synthase in TLR4-competent mice, whereas increased parasite survival in host cells from TLR4-deficient mice correlates with a higher activity of arginase, an enzyme known to promote parasite growth. This is the first study showing that TLR4 contributes to the effective control ofLeishmaniainfection in vivo.
Immunoglobulin-Mediated Agglutination of and Biofilm Formation by
Escherichia coli
K-12 Require the Type 1 Pilus Fiber
Authors: Orndorff Paul E. , Devapali Aditya , Palestrant Sarah , Wyse Aaron , Everett Mary Lou , Bollinger R. Randal , Parker William 
Published: March 2004

ABSTRACT

The binding of human secretory immunoglobulin A (SIgA), the primary immunoglobulin in the gut, to
Escherichia coli
is thought to be dependent on type 1 pili. Type 1 pili are filamentous bacterial surface attachment organelles comprised principally of a single protein, the product of the
fimA
gene. A minor component of the pilus fiber (the product of the
fimH
gene, termed the adhesin) mediates attachment to a variety of host cell molecules in a mannose inhibitable interaction that has been extensively described. We found that the aggregation of
E. coli
K-12 by human secretory IgA (SIgA) was dependent on the presence of the pilus fiber, even in the absence of the mannose specific adhesin or in the presence of 25 mM α-CH
3
Man. The presence of pilus without adhesin also facilitated SIgA-mediated biofilm formation on polystyrene, although biofilm formation was stronger in the presence of the adhesin. IgM also mediated aggregation and biofilm formation in a manner dependent on pili with or without adhesin. These findings indicate that the pilus fiber, even in the absence of the adhesin, may play a role in biologically important processes. Under conditions in which
E. coli
was agglutinated by SIgA, the binding of SIgA to
E. coli
was not increased by the presence of the pili, with or without adhesin. This observation suggests that the pili, with or without adhesin, affect factors such as cell surface rigidity or electrostatic repulsion, which can affect agglutination but which do not necessarily determine the level of bound immunoglobulin.
Lon Protease Activity Causes Down-Regulation of
Salmonella
Pathogenicity Island 1 Invasion Gene Expression after Infection of Epithelial Cells
Authors: Boddicker Jennifer D. , Jones Bradley D. 
Published: March 2004

ABSTRACT

Salmonella enterica
serovar Typhimurium causes self-limiting gastroenteritis in humans and a typhoid-like disease in mice that serves as a model for typhoid infections in humans. A critical step in
Salmonella
pathogenesis is the invasion of enterocytes and M cells of the small intestine via expression of a type III secretion system, encoded on
Salmonella
pathogenicity island 1 (SPI-1), that secretes effector proteins into host cells, leading to engulfment of the bacteria within large membrane ruffles. The in vitro regulation of invasion genes has been the subject of much scientific investigation. Transcription of the
hilA
gene, which encodes an OmpR/ToxR-type transcriptional activator of downstream invasion genes, is increased during growth under high-osmolarity and low-oxygen conditions, which presumably mimic the environment found within the small intestine. Several negative regulators of invasion gene expression have been identified, including HilE, Hha, and Lon protease. Mutations within the respective genes increase the expression of
hilA
when the bacteria are grown under environmental conditions that are not favorable for
hilA
expression and invasion. In this study, the intracellular expression of invasion genes was examined, after bacterial invasion of HEp-2 epithelial cells, using
Salmonella
strains containing plasmid-encoded short-half-life green fluorescent protein reporters of
hilA
,
hilD
,
hilC
, or
sicA
expression. Interestingly, the expression of SPI-1 genes was down-regulated after invasion, and this was important for the intracellular survival of the bacteria. In addition, the effects of mutations in genes encoding negative regulators of invasion on intracellular
hilA
expression were examined. Our results indicate that Lon protease is important for down-regulation of
hilA
expression and intracellular survival after the invasion of epithelial cells.
Analysis of Relative Levels of Production of Pertussis Toxin Subunits and Ptl Proteins in
Bordetella pertussis
Authors: Cheung Anissa M. , Farizo Karen M. , Burns Drusilla L. 
Published: March 2004

ABSTRACT

Pertussis toxin is transported across the outer membrane of
Bordetella pertussis
by the type IV secretion system known as the Ptl transporter, which is composed of nine different proteins. In order to determine the relative levels of production of pertussis toxin subunits and Ptl proteins in
B. pertussis
, we constructed translational fusions of the gene for alkaline phosphatase,
phoA
, with various
ptx
and
ptl
genes. Comparison of the alkaline phosphatase activity of strains containing
ptx
′- or
ptl
′-
phoA
fusions indicated that pertussis toxin subunits are produced at higher levels than Ptl proteins, which are encoded by genes located toward the 3′ end of the
ptx-ptl
operon. We also engineered strains of
B. pertussis
by introducing multiple copies of the
ptl
genes or subsets of these genes and then examined the ability of each of these strains to secrete pertussis toxin. From these studies, we determined that certain Ptl proteins appear to be limiting in the secretion of pertussis toxin from the bacteria. These results represent an important first step in assessing the stoichiometric relationship of pertussis toxin and its transporter within the bacterial cell.
Phagocytosis of Apoptotic Cells Increases the Susceptibility of Macrophages to Infection withCoxiella burnetiiPhase II through Down-Modulation of Nitric Oxide Production
Authors: Zamboni Dario S. , Rabinovitch Michel 
Published: March 2004

ABSTRACTCoxiella burnetii, the agent of Q fever in humans and coxiellosis in other mammals, is an obligate intracellular bacterium which is sheltered and multiplies within typically large phagolysosome-like replicative vacuoles (LRVs). We have previously shown that, compared with fibroblasts, mouse resident peritoneal macrophages control the development of LRVs and bacterial multiplication within these vacuoles. Earlier experiments with the nitric oxide (NO) synthase inhibitor aminoguanidine (AG) revealed that the control is exerted by NO induced by the bacteria. We report here that phagocytosis of apoptotic-like, but not of aldehyde-killed, lymphocytes by the macrophages reduced the production of NO induced by the bacteria and increased the development of LRVs and, therefore, the total bacterial load in the cultures. Experiments with macrophages from mice deficient for inducible NO synthase (iNOS−/−) confirmed the involvement of NO in the control of infection, since neither apoptotic lymphocytes nor AG affected the development of LRVs in these phagocytes. Since macrophages are important for the clearance of apoptotic bodies andC. burnetiiis able to induce apoptosis in human monocytes, the phenomenon shown here may be biologically relevant to the development of Q fever and coxiellosis.
Vaccine Potential of theNeisseria meningitidis2086 Lipoprotein
Authors: Fletcher Leah D. , Bernfield Liesel , Barniak Vicki , Farley John E. , Howell Alan , Knauf Melissa , Ooi Peggy , Smith Robert P. , Weise Paige , Wetherell Mike , Xie Xiaoling , Zagursky Robert , Zhang Ying , Zlotnick Gary W. 
Published: March 2004

ABSTRACTA novel antigen that induces cross-reactive bactericidal antibodies against a number ofNeisseria meningitidisstrains is described. This antigen, a ∼28-kDa lipoprotein called LP2086, was first observed within a complex mixture of soluble outer membrane proteins (sOMPs) following a series of fractionation, protein purification, and proteomics steps. Approximately 95 different neisserial isolates tested positive by Western blotting and PCR screening methods for the presence of the protein and the gene encoding LP2086. The strains tested included isolates ofN. meningitidisserogroups A, B, C, W135, and Y,Neisseria gonorrhoeae, andNeisseria lactamica. To better understand the microheterogeneity of this protein, the 2086 genes from 63 neisserial isolates were sequenced. Two different subfamilies of LP2086 were identified based on deduced amino acid sequence homology. A high degree of amino acid sequence similarity exists within each 2086 subfamily. The highest degree of genetic diversity was seen between the two subfamilies which share approximately 60 to 75% homology at the nucleic acid level. Flow cytometry (fluorescence-activated cell sorting) analyses and electron microscopy indicated that the LP2086 is localized on the outer surface ofN. meningitidis. Antiserum produced against a single protein variant was capable of eliciting bactericidal activity against strains expressing different serosubtype antigens. Combining one recombinant lipidated 2086 (rLP2086) variant from each subfamily with two rPorA variants elicited bactericidal activity against all strains tested. The rLP2086 family of antigens are candidates worthy of further vaccine development.
Toll-Like Receptor 2 Is Required for Optimal Control ofListeria monocytogenesInfection
Authors: Torres David , Barrier Mathieu , Bihl Franck , Quesniaux Valerie J. F. , Maillet Isabelle , Akira Shizuo , Ryffel Bernhard , Erard François 
Published: March 2004

ABSTRACTThe control ofListeria monocytogenesinfection depends on the rapid activation of the innate immune system, likely through Toll-like receptors (TLR), since mice deficient for the common adapter protein of TLR signaling, myeloid differentiation factor 88 (MyD88), succumb toListeriainfection. In order to test whether TLR2 is involved in the control of infections, we compared the host response in TLR2-deficient mice with that in wild-type mice. Here we show that TLR2-deficient mice are more susceptible to systemic infection byListeriathan are wild-type mice, with a reduced survival rate, increased bacterial burden in the liver, and abundant and larger hepatic microabscesses containing increased numbers of neutrophils. The production of tumor necrosis factor, interleukin-12, and nitric oxide and the expression of the costimulatory molecules CD40 and CD86, which are necessary for the control of infection, were reduced in TLR2-deficient macrophages and dendritic cells stimulated byListeriaand were almost abolished in the absence of MyD88, coincident with the high susceptibility of MyD88-deficient mice to in vivo infection. Therefore, the present data demonstrate a role for TLR2 in the control ofListeriainfection, but other MyD88-dependent signals may contribute to host resistance.
Effect of Bronchoalveolar Lavage Fluid fromPneumocystis carinii- Infected Hosts on Phagocytic Activity of Alveolar Macrophages
Authors: Lasbury Mark E. , Lin Peimao , Tschang Dennis , Durant Pamela J. , Lee Chao-Hung 
Published: March 2004

ABSTRACTAlveolar macrophages fromPneumocystis carinii-infected rats are defective in phagocytosis. To investigate whether this defect is due to a certain factor present inP. carinii-infected lungs, alveolar macrophages from uninfected rats were incubated with bronchoalveolar lavage (BAL) fluid samples fromP. carinii-infected rats. Alveolar macrophages treated with these BAL fluid samples became defective in phagocytosis but remained normal when treated with BAL fluid samples from noninfected orToxoplasma gondii-infected rats. The suppressive activity of the BAL fluid samples fromP. carinii-infected rats on phagocytosis was retained when the BAL fluid samples were passed through a filter with a pore size of 0.45 μm but was lost when the BAL fluid samples were digested with proteases such as trypsin, pepsin, papain, or endopeptidase Gly-C. Lipid fractions of these BAL fluid samples had no suppressive activity on phagocytosis. The suppressive activity of these BAL fluid samples was also lost when they were incubated with concanavalin A-agarose beads, suggesting that the inhibitor is a glycoprotein. The inhibitor was estimated to be larger than 100,000 Da by exclusion filtration. After binding to the concanavalin A-agarose beads, the inhibitor in BAL fluid samples andP. cariniilysate could be eluted with 200 mM methylmannose. Treatment of both the crude BAL fluid samples andP. cariniilysate and the 200 mM methylmannose eluate with antibody against the major surface glycoprotein ofP. cariniieliminated their suppressive activity. These results suggest that the factor capable of suppressing the phagocytic activity of alveolar macrophages isP. cariniimajor surface glycoprotein or one or more of its derivatives.
Normally Occurring Human Anti-GM1Immunoglobulin M Antibodies and the Immune Response to Bacteria
Authors: Alaniz María E. , Lardone Ricardo D. , Yudowski Silvia L. , Farace María I. , Nores Gustavo A. 
Published: March 2004

ABSTRACTAnti-GM1antibodies of the immunoglobulin M (IgM) isotype are normal components of the antibody repertoire of adult human serum. Using a sensitive high-performance thin-layer chromatography (HPTLC) immunostaining assay, we found that these antibodies were absent in the umbilical vein and children <1 month of age but could be detected after 1 month of age. Although most of the children older than 6 months of age were positive, there were still a few negative children. The appearance of anti-GM1IgM antibodies showed a perfect concordance with two well-characterized antibacterial antibodies, anti-Forssman and anti-blood group A, which indicates a similar origin. We also studied IgM reactivity with lipopolysaccharides (LPSs) from gram-negative bacteria isolated from stool samples from healthy babies and fromEscherichia coliHB101 in serum from individuals of different ages. We found a positive reaction with both LPSs in all the children more than 1 month of age analyzed, even in those that were negative for anti-GM1antibodies. Anti-GM1IgM antibodies were purified from adult serum by affinity chromatography and tested for the ability to bind LPSs from different bacteria. This highly specific preparation showed reactivity only with LPS from a strain ofCampylobacter jejuniisolated from a patient with diarrhea. We conclude that normally occurring IgM antibodies are generated after birth, probably during the immune defense against specific bacterial strains.
Detergent-Resistant Membrane Microdomains Facilitate Ib Oligomer Formation and Biological Activity of
Clostridium perfringens
Iota-Toxin
Authors: Hale Martha L. , Marvaud Jean-Christophe , Popoff Michel R. , Stiles Bradley G. 
Published: March 2004

ABSTRACT

Clostridium perfringens
iota-toxin consists of two separate proteins identified as a cell binding protein, iota b (Ib), which forms high-molecular-weight complexes on cells generating Na
+
/K
+
-permeable pores through which iota a (Ia), an ADP-ribosyltransferase, presumably enters the cytosol. Identity of the cell receptor and membrane domains involved in Ib binding, oligomer formation, and internalization is currently unknown. In this study, Vero (toxin-sensitive) and MRC-5 (toxin-resistant) cells were incubated with Ib, after which detergent-resistant membrane microdomains (DRMs) were extracted with cold Triton X-100. Western blotting revealed that Ib oligomers localized in DRMs extracted from Vero, but not MRC-5, cells while monomeric Ib was detected in the detergent-soluble fractions of both cell types. The Ib protoxin, previously shown to bind Vero cells but not form oligomers or induce cytotoxicity, was detected only in the soluble fractions. Vero cells pretreated with phosphatidylinositol-specific phospholipase C before addition of Ib indicated that glycosylphosphatidyl inositol-anchored proteins were minimally involved in Ib binding or oligomer formation. While pretreatment of Vero cells with filipin (which sequesters cholesterol) had no effect, methyl-β-cyclodextrin (which extracts cholesterol) reduced Ib binding and oligomer formation and delayed iota-toxin cytotoxicity. These studies showed that iota-toxin exploits DRMs for oligomer formation to intoxicate cells.
Identification and Molecular Characterization of a Gene Encoding a ProtectiveLeishmania amazonensisTrp-Asp (WD) Protein
Authors: Campbell Kimberly , Popov Vsevolod , Soong Lynn 
Published: March 2004

ABSTRACTSeveralLeishmaniaproteins have been identified and characterized in pursuit of understanding pathogenesis and protection in cutaneous leishmaniasis. In the present study, we utilized sera from infected BALB/c mice to screen aLeishmania amazonensisamastigote cDNA expression library and obtained the full-length gene that encodes a novel Trp-Asp (WD) protein designated LAWD (forLeishmaniaantigenic WD protein). The WD family of proteins mediates protein-protein interactions and coordinates the formation of protein complexes. The single-copy LAWD gene is transcribed as a ∼3.1-kb mRNA in both promastigotes and amastigotes, with homologues being detected in several otherLeishmaniaspecies. Immunoelectron microscopy revealed a predominant localization of the LAWD protein in the flagellar pocket. Analyses of sera from human patients with cutaneous and mucocutaneous leishmaniasis indicated that these individuals mounted significant humoral responses against LAWD. Given that recombinant LAWD protein elicited the production of high levels of gamma interferon, but no detectable levels of interleukin-10 (IL-10), in CD4+cells ofL. amazonensis-infected mice, we further examined whether LAWD could elicit protective immunity. DNA vaccination with the LAWD and IL-12 genes significantly delayed lesion development, which correlated with a dramatic reduction in parasite burdens. Thus, we have successfully identified a promising vaccine candidate and antigenic vehicle to aid in the dissection of the complicated pathogenic immune response ofL. amazonensis.