bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fracture resistance of incisor teeth restored using fibre‐reinforced posts and threaded metal posts: effect of post length, location, pretreatment and cementation of the final restoration
Authors: Schmitter M. , Lippenberger S. , Rues S. , Gilde H. , Rammelsberg P. 
Published: April 2010

Schmitter M, Lippenberger S, Rues S, Gilde H, Rammelsberg P. Fracture resistance of incisor teeth restored using fibre‐reinforced posts and threaded metal posts: effect of post length, location, pretreatment and cementation of the final restoration. International Endodontic Journal, 43, 436–442, 2010.AbstractObjective  The hypothesis of this study was that the fracture load of incisor teeth restored using short, threaded, parallel‐sided posts (TMP) is, under special conditions, not inferior to that of teeth restored using long TMPs or fibre‐reinforced posts (FRP).Methodology  Seventy‐two maxillary incisors and 72 mandibular incisors were collected. Sixty‐four in each group were root filled; in half of these FRPs were cemented, and in the other half TMPs were used. Half of the FRPs were pretreated; the others were not pretreated. In the TMP‐group, half of the teeth received a long post (10 mm), the other half a short post (3 mm). Crowns were fabricated and cemented with Ketac‐cem or Panavia. Eight maxillary incisors and eight mandibular incisors with intact natural crowns were used as control groups. All specimens were loaded until fracture.Results  Fracture loads were higher for pretreated FRPs than for untreated FRPs. If the FRPs were not pretreated, fracture loads for maxillary incisors after use of short metal posts were significantly higher (248 N compared with 133 N, P = 0.027). Fracture loads for teeth restored using long TMPs were not higher than for teeth restored using short TMPs (277 N compared with 266 N). Fracture loads for mandibular incisors restored using long (10 mm) pretreated FRP were higher than for mandibular incisors restored using short (3 mm) metal posts (436 N compared with 285 N). Cementation of the crowns using an adhesive resin cement did not increase the fracture load for mandibular incisors, whereas for maxillary incisors, this cementation technique tended to increase fracture loads in teeth restored with FRP, although this increase was not significant at the P < 0.05 level (P = 0.06). In both groups, fracture loads were higher for mandibular incisors.Conclusions  Short, threaded, parallel‐sided metal posts might be an alternative to fibre‐ reinforced posts for maxillary incisors, for teeth with short roots or when FRP cannot be pretreated.
Essential lysine residues within transmembrane helix 1 of diphtheria toxin facilitate COPI binding and catalytic domain entry
Authors: Trujillo Carolina , Taylor‐Parker Julian , Harrison Robert , Murphy John R. 
Published: April 2010

SummaryThe translocation of the diphtheria toxin catalytic domain from the lumen of early endosomes into the cytosol of eukaryotic cells is an essential step in the intoxication process. We have previously shown that the in vitro translocation of the catalytic domain from the lumen of toxin pre‐loaded endosomal vesicles to the external medium requires the addition of cytosolic proteins including coatomer protein complex I (COPI) to the reaction mixture. Further, we have shown that transmembrane helix 1 plays an essential, but as yet undefined role in the entry process. We have used both site‐directed mutagenesis and a COPI complex precipitation assay to demonstrate that interaction(s) between at least three lysine residues in transmembrane helix 1 are essential for both COPI complex binding and the delivery of the catalytic domain into the target cell cytosol. Finally, a COPI binding domain swap was used to demonstrate that substitution of the lysine‐rich transmembrane helix 1 with the COPI binding portion of the p23 adaptor cytoplasmic tail results in a mutant that displays full wild‐type activity. Thus, irrespective of sequence, the ability of transmembrane helix 1 to bind to COPI complex appears to be the essential feature for catalytic domain delivery to the cytosol.
Cellular Expression or Binding of desLys58‐β2 Microglobulin is not Dependent on the Presence of the Tri‐molecular MHC Class I Complex
Authors: Wang M. , Corlin D. B. , Heegaard N. H. H. , Claesson M. H. , Nissen M. H. 
Published: April 2010

AbstractThe monoclonal antibody 332‐01 is a newly developed antibody which specifically recognizes human desLys58‐β2 microglobulin (dβ2m). In the present study, we characterized the binding of 332‐01 to peripheral blood mononuclear cells (PBMC), a number of human leukaemic and monocytic cell lines, and β2m gene‐deleted murine lymphocytes. dβ2m was found to be expressed on non‐activated and activated monocytes. When cells were pre‐exposed to dβ2m, 332‐01 also bound to non‐activated T lymphocytes. dβ2m was expressed on the monocytic cell lines U937 and TIB‐202, and binding was significantly increased when cells were pre‐incubated with dβ2m and when TIB‐202 cells were exposed to lipopolysaccharide. dβ2m was also expressed on T leukaemic Jurkat cells as well as on low HLA‐expressing erythroleukaemic K562 cells. β2m gene‐deleted murine splenocytes only bound 332‐01 after pre‐exposure to dβ2m. Binding of 332‐01 antibody could not be displaced by addition of high concentrations of native β2m. In conclusion, our data indicate that dβ2m – in contrast to native β2m – binds to a hitherto unknown cell surface receptor independent of classical MHC class I molecules. As β2m has previously been shown to display biological activities such as the induction of both growth promotion and apoptosis, C1 complement activity, shown to mediate cleavage of β2m, could be involved in these processes.
Breaking B‐cell Tolerance and CTL Tolerance in three OVA‐transgenic Mouse Strains Expressing Different Levels of OVA
Authors: Steinaa L. , Rasmussen P. B. , Gautam A. , Mouritsen S. 
Published: April 2010

AbstractIt is of major importance to overcome the immunological tolerance in attempts to generate efficient tumour vaccines. Here, we describe induction of autoantibodies and self‐reactive CTL in three types of OVA‐transgenic mouse strains, RIP‐OVAlow, RIP‐mOVA and RIP‐OVAHI exhibiting varying levels of OVA expression and tolerance. This was achieved by immunizing with DNA constructs where a foreign T‐helper epitope, P30 from tetanus toxin, was inserted into the OVA sequence. OVA wild‐type DNA as well as the P30‐modified OVA DNA vaccines (OVA‐P30) were constructed and used for immunization in the OVA‐transgenic mouse strains as well as in control C57Bl/6 mice. The data show that insertion of a foreign T‐helper peptide (P30) in OVA is sufficient for breaking B‐cell tolerance in three different OVA‐transgenic mice strain. This approach is sufficient for induction of self‐reactive CTL in two of the three strains that expressed either a membrane‐bound form of OVA or a low amount of soluble OVA. It was not possible to induce CTL but still possible to induce autoantibodies in the strain that expressed a higher level of soluble OVA.
Macrophage Migration Inhibitory Factor Has a MHC class I‐Like Motif and Function
Authors: Gibbings D. J. , Ghetu A. F. , Dery R. , Befus A. D. 
Published: April 2010

AbstractMacrophage migration inhibitory factor (MIF) is found in immune‐privileged sites and inhibits cytotoxicity mediated by CD3‐ve lymphokine‐activated killer cells (LAK). The mechanism by which MIF attenuates LAK cytotoxicity is unknown. We provide evidence that MIF has a major histocompatibility complex (MHC) class I‐like motif. A monoclonal antibody (OX18) that binds a conserved region of rat MHC class I proteins binds native MIF. Anti‐MIF polyclonal antibodies bind MHC class I. Epitope mapping suggests OX18 binds a loop of MHC class I bound by several receptors for MHC class I. A sequence (PRPEG) within the proposed OX18‐binding site on MHC class I exists with a short insertion in MIF. OX18 does not bind MIF that is denatured by SDS‐PAGE. This suggests the OX18 epitope is dependent on higher order structure in MIF. Interestingly, MIF inhibits binding of tetramers of MHC class I (H2Db) to LAK cells, suggesting it may bind to receptors for MHC class I. MIF may be an example where small regions of MHC class I are used by endogenous and viral proteins to control cytotoxicity mediated by immune cells.
Naturally Acquired Immunity and Reduced Susceptibility to falciparum Malaria in Two Subpopulations of Endemic Eastern India
Authors: Biswas S. , Seth R. K. , Tyagi P. K. , Sharma S. K. , Dash A. P. 
Published: April 2010

AbstractThis study was aimed to assess the prevalence of naturally acquired humoral immune responses and their association with reduced susceptibility to malaria in children and adults with differential clinical conditions from an Indian zone where malaria is endemic. The study was undertaken in an eastern province of India (Keonjhar, Orissa) in a group of 341 children (both younger and older) and 98 adults living in two different areas, Town area and Forest area. They were studied for their parasitological and immunological profiles. Sera from different age‐matched groups were screened by ELISA to measure IgG reactivities for characterizing humoral immune responses to the B‐cell epitopes of Plasmodium falciparum MSP1, AMA1, RAP1 and EBA175 peptides and P. falciparum‐infected erythrocyte lysate. In Town area, overall P. falciparum cases were 5.5%, whereas those in Forest area were 26.7%. We observed an age‐wise increasing trend of immunity in these two populations. It was also noticed that the frequency of responders to stage‐specific antigens was higher in individuals from the Town area where the frequency of malaria was lower. The naturally acquired humoral immune responses to different stage‐specific antigens of P. falciparum reflect the reduced risk of malaria in the study groups. The higher frequency of seroresponders showed correlation with lower risk of developing malaria.
Evaluation of a new Recombinant BCG which Contains Mycobacterial Antigen ag85B–mpt64190–198–mtb8.4 in C57/BL6 Mice
Authors: Qie Y. Q. , Wang J. L. , Zhu B. D. , Xu Y. , Wang Q. Z. , Chen J. Z. , Wang H. H. 
Published: April 2010

AbstractTuberculosis (TB) caused by Mycobacterium tuberculosis continues to be one of the major public health problems in the world. The eventual control of this disease will require the development of a safe and effective vaccine. Bacille Calmette‐Guerin (BCG), the only vaccine against TB, is not perfect for its limited ability to protect against the adult form of TB. Some improvements of TB vaccines relied to strengthening the immunogenicity and/or persistence of genetically modified recombinant BCG (rBCG) strain. Antigen 85B (Ag85B) and Mtb8.4 are importantly immunodominant antigens of M. tuberculosis, and both are very promising vaccine candidate molecules. MPT64190–198, is presented to CD8+ T cells during mycobacterial infections. In this study, we combined these above genes into one recombinant gene of ag85B–mpt64190–198–mtb8.4. Then we constructed the new rBCG containing this united gene. This rBCG can induce an increased Th1‐type immune response in mice, characterized by an elevated level of interferon‐γ in antigen‐stimulated splenocyte culture and a strong IgG2a antibody response. Also, it can elicit longer immune responses than BCG. The results show that this rBCG is a promising candidate for further study.
B‐cell Activating Factor of the Tumour Necrosis Factor Family Expression in Blood Monocytes and T Cells from Patients with Primary Sjögren’s Syndrome
Authors: Lavie F. , Miceli‐Richard C. , Ittah M. , Sellam J. , Gottenberg J.‐E. , Mariette X. 
Published: April 2010

AbstractWe investigated B‐cell activating factor of the tumour necrosis factor family (BAFF) level in peripheral blood mononuclear cells (PBMCs), monocytes and T cells from patients with primary Sjögren’s syndrome (pSS) and controls both ex vivo and in vitro after cytokine stimulation. PBMCs, monocytes and T cells were isolated from 15 patients with pSS and 17 controls. Cells were cultured alone or with interferon (IFN)α, IFNγ and interleukin 10 (IL‐10). T cells were stimulated with phytohaemagglutin and anti‐CD3. BAFF protein was assessed by enzyme‐linked immunosorbent assay. Ex vivo, no difference was observed in BAFF mRNA level in PBMCs and monocytes from patients and controls. Blood monocytes were the main cell type secreting BAFF both in patients and controls. In vitro, after IFNα stimulation, BAFF mRNA level was significantly higher in cells from patients than from controls (63.8 versus 20.7, P = 0.03). T cells from patients secreted a higher level of BAFF protein than those from healthy donor cells (17.4 versus 2.9 pg/ml, respectively, P = 0.04) but at a lower level than that from monocytes. Stimulation of T cells did not change BAFF secretion level. The induction of Th17 cells showed no increased BAFF expression. In conclusion, similar to epithelial cells, blood monocytes in patients with pSS show increased production of BAFF under IFNα, which confirms the involvement of IFNα in pSS. BAFF expression is also increased in blood T cells of such patients, independently of T‐cell stimulation.
Suppression of Allergic Inflammation by Allergen‐DNA‐modified Dendritic Cells Depends on the Induction of Foxp3+ Regulatory T Cells
Authors: Wu Kui , Bi Yuttian , Sun Kun , Xia Junbo , Wang Yan , Wang Changzheng 
Published: April 2010

AbstractCD4+CD25+Foxp3+Regulatory T cells (Tregs) play important roles in regulating allergic inflammation. To analyse if allergen‐DNA‐modified dendritic cells (DC) can suppress allergic responses and what roles Treg cells play in DC‐based allergen‐specific immunotherapy. Immature DC were transfected with retrovirus encoding Der p2 DNA, and administered to mice that sensitized and challenged with Der p2 protein. After Treg cells were depleted with anti‐CD25 mAb, mice were re‐challenged to observe the airway inflammation, and Treg cells in spleen CD4+ T cells. And responses of spleen CD4+ T cells to Der p2 were determined. Co‐culture of naïve CD4+ T cells with allergen‐modified DC induced Foxp3+ Tregs. Sensitized and challenged mice developed allergic airway inflammation and Th2 responses, and decreased Foxp3+ Tregs. Treatment with allergen‐modified‐DC suppressed airway inflammation and Th2 responses, and increased IL‐10 and IFN‐γ production and Foxp3+ Tregs significantly; and eliminated the responses of CD4+ T cells to allergen. Administration of anit‐CD25 mAb eliminated all the effects of modified‐DC except for the increasing of IFN‐γ. Allergen‐modified DC can induce immune tolerance to allergens and reverse the established Th2 responses induced by allergen, with dependence on the induction of Foxp3+ Tregs.
Peripheral Blood CD14high CD16+ Monocytes are Main Producers of IL‐10
Authors: Skrzeczyńska‐Moncznik J. , Bzowska M. , Lo˝seke S. , Grage‐Griebenow E. , Zembala M. , Pryjma J. 
Published: April 2010

AbstractBased on CD14 and CD16 expression, human peripheral blood monocytes (MO) can be divided into a major CD14high CD16− population and two minor CD14high CD16+ and CD14dim CD16+ subpopulations. CD14dim CD16+ MO are well characterized and regarded as pro‐inflammatory because upon stimulation produce TNF‐α but little, if any, IL‐10. By contrast, little is known about CD14high CD16+ MO. We investigated the surface expression of selected determinants by CD16+ MO subpopulations, cytokine production, phagocytosis and antigen presentation. We found that both CD16+ subpopulations had a higher expression of HLA‐DR, CD86, CD54 and a lower expression of CD64 than CD14high CD16− population. In addition, CD14high CD16+ MO showed a higher expression of CD11b and TLR4 than CD14dim CD16+ and CD14high CD16− subpopulations. CD14high CD16+ MO exhibited an increased phagocytic activity and a decreased antigen presentation in comparison with CD14dim CD16+. As expected, lipopolysaccharide (LPS)‐stimulated CD14dim CD16+ MO produced TNF‐α but little IL‐10. By contrast, LPS‐stimulated CD14high CD16+ subpopulation produced significantly more IL‐10 than CD14dim CD16+ and CD14high CD16− MO. In conclusion, our data show that human peripheral blood CD16+ MO are heterogeneous in function and consist of two subpopulations: CD14dim CD16+ pro‐inflammatory and CD14high CD16+ with anti‐inflammatory potential.
The Effect of Specific MHC Class I and Class II Combinations on Resistance to Furunculosis in Atlantic Salmon (Salmo salar)
Authors: Kjøglum S. , Larsen S. , Bakke H. G. , Grimholt U. 
Published: April 2010

AbstractThe aim was to evaluate the performance of selected individual major histocompatibility complex (MHC) class I and class II alleles and combinations of these on disease resistance against furunculosis. The material, consisting of 2,145 Atlantic salmon (Salmo salar) from seven families, contained four MHC class I (UBA) alleles and two MHC class II alpha (DAA) alleles. The included alleles were previously shown to influence resistance towards furunculosis. The fish were challenged with the bacterium Aeromonas salmonicidae, causing furunculosis. The total mortality in the material was 84.0%, and both dead and surviving fish were genotyped for UBA and DAA. For MHC class II fish with DAA*0301 were more resistant than fish with DAA*0201, which were significantly more susceptible (P < 0.05). For MHC class I, the ranking of performance of the alleles differed from previous results, and fish with allele UBA*0601 were found to be most resistant while fish with UBA*0501, UBA*0201 and UBA*0301 were more susceptible. The analysis of combined MHC class I and class II genotype detected that fish with genotypes UBA*0501/*0501;DAA*0301/*0301, UBA*0601/*0601;DAA*0301/*0301 and UBA*0601/*0601;DAA*0201/*0201 were most resistant (P < 0.05), while the genotypes associated with increased susceptibility were UBA*0501/*0501; DAA*0201/*0301 and UBA*0501/*0501;DAA*0201/*0201 (P < 0.05). In addition, Cox regression analysis show that both family and MHC alleles contributed significantly to survival. Thus, in addition to reproducing the effect on resistance and susceptibility of many MHC class I and class II alleles individually, we also detected an effect of certain MHC class I and class II combinations suggestive of cross‐talk between the class I and class II pathways.
TNF‐alpha Induction by Pseudomonas aeruginosa Lipopolysaccharide or Slime‐glycolipoprotein in Human Monocytes is Regulated at the Level of Mitogen‐activated Protein Kinase Activity: A Distinct Role of Toll‐like Receptor 2 and 4
Authors: Lagoumintzis G. , Xaplanteri P. , Dimitracopoulos G. , Paliogianni F. 
Published: April 2010

AbstractTNF‐α production has a central role in the development and progression of Pseudomonas aeruginosa septic shock. We have previously shown that P. aeruginosa slime‐glycolipoprotein (slime‐GLP) is the most potent stimulant compared to P. aeruginosa lipopolysaccharide (LPS), for TNF‐α production and NF‐kB activation in human monocytes. Herein, we show that secretion of TNF‐α by fresh human monocytes, induced by P. aeruginosa slime‐GLP, LPS or viable bacteria, was paralleled by phosphorylation and/or activation of Mitogen‐activated Protein Kinases (MAPKs) ERK1/2, p38 as well as c‐Jun NH2‐terminal kinase. TNF‐α levels were significantly reduced by ERK1/2 inhibitor (PD98059), or p38 inhibitor (SB203580). Combination of both inhibitors almost abolished TNF‐α induction. Pseudomonas aeruginosa slime‐GLP differed from the P. aeruginosa‐LPS only regarding the strength of p38 and ERK1/2 activation, with slime‐GLP leading to a stronger activation of p38 and ERK1/2. Involvement of TLR2 and TLR4 for phosphorylation of p38 and ERK1/2 was shown using specific blocking anti‐TLR2 and anti‐TLR4 antibodies. Activation of both p38 and ERK1/2 induced by P. aeruginosa slime‐GLP was dramatically reduced in the presence of anti‐TLR2 and to a lesser degree in the presence of anti‐TLR4, whereas the P. aeruginosa‐LPS‐induced stimulation was inhibited only in the presence of anti‐TLR4. Our data show that P. aeruginosa viable bacteria, through slime‐GLP, stimulate specific members of the MAPKs more efficiently than the P. aeruginosa‐LPS, involving mainly TLR2.
Interleukin‐12 and Tumour Necrosis Factor‐α Equilibrium is a Prerequisite for Clinical Course Free from Late Complications in Children with Type 1 Diabetes Mellitus
Authors: Zorena K. , Myśliwska J. , Myśliwiec M. , Balcerska A. , Lipowski P. , Raczyńska K. 
Published: April 2010

AbstractThe objective of the study was to analyse levels of IL‐12 and TNF‐α and relate the findings to the occurrence of microangiopathy in children with type 1 diabetes mellitus (DM). We examined a group of 123 children with type 1 DM. Serum levels of IL‐12 and TNF‐α were measured by an immunoenzymatic ELISA technique. TNF‐α and IL‐12 tended to be simultaneously present or absent in the sera of 50% of the children who had not developed complications, thus indicating a state of cytokine’s equilibrium. Among the patients with an established retinopathy, two IL‐12/TNF‐α combinations were visible. Either a lack of detectable TNF‐α was accompanied by measurable IL‐12 serum concentrations or TNF‐α incidence was associated with undetectable IL‐12 values. Simultaneous lack of TNF‐α and presence of IL‐12 was associated with a better prognosis as these patients had a significantly lower albumin excretion rate. The state of equilibrium between TNF‐α and IL‐12 is beneficial in patients at early stages of the disease, prior to the occurrence of complications. Shifting the equilibrium towards TNF‐α seems to promote late complications. It may suggest that a disharmony between pro‐ and anti‐angiogenic function of these cytokines underlie the mechanism by which TNF‐α and IL‐12 shape the disease course.
Internalization of Staphylococcus aureus by Bovine Endothelial Cells is Associated with the Activity State of NF‐κB and Modulated by the Pro‐inflammatory Cytokines TNF‐α and IL‐1β
Authors: Oviedo‐Boyso J. , Barriga‐Rivera J. G. , Valdez‐Alarcón J. J. , Bravo‐Patiño A. , Cárabez‐Trejo A. , Cajero‐Juárez M. , Baizabal‐Aguirre V. M. 
Published: April 2010

AbstractBacterial internalization is an important process in the pathogenesis of infectious diseases in which nuclear factor kappaB (NF‐κB) plays a prominent role. We present pharmacological evidence indicating that in bovine endothelial cells (BEC) the internalization of Staphylococcus aureus, a pathogenic bacterium that causes mastitis in bovine cattle, was associated with the activation of NF‐κB. The internalization of S. aureus increased when BEC were stimulated with alpha‐tumour necrosis factor (TNF‐α) or beta‐interleukin 1 (IL‐1β) which are known activators of NF‐κB. SN50 (an inhibitor peptide of NF‐κB nuclear translocation) and BAY 11‐7083 (a chemical that inhibits the IκBα phosphorylation) caused significant reduction in S. aureus intracellular number, indicating that its internalization was associated with the NF‐κB activity. Furthermore, specific inhibition of c‐Jun N‐terminal kinase with SP600125 (SP) or p‐38 with SB203580 (SB) did not cause any change in the S. aureus intracellular number compared with the untreated control. Finally, TNF‐α treatment of BEC after the addition of both SP and SB, induced a significant increase in S. aureus internalization above the control value. These data indicate that NF‐κB activity is associated with S. aureus internalization and suggest that this transcription factor may play a role in the pathophysiology of bovine mastitis caused by this bacterium.