PubMed Health⌕ Search

Biomedical subjects

D Vidović

Publications and source records attributed to D Vidović.

At least 19 recordsLinked to original sources
PubMed2006

Factors affecting recurrence after incisional hernia repair.

Incisional hernias occur primarily as a result of high tension and inadequate healing of a previous incision, the latter of which is frequently related to infection at the surgical site. Despite recent advances in operative techniques, the recurrence rate remains unacceptably high. To evaluate the impact of different predisposing factors for the recurrence of incisional hernia, we reviewed retrospectively the medical records of 297 patients who had undergone incisional herniorrhaphy (188 tissue repairs, 109 mesh repairs) in our hospital. Demographic data (age and gender), type of repair, body mass index, hernia size, presence of chronic illnesses and wound complications were evaluated in a univariate and multivariate manner analysis. The overall recurrence rate was 30.3%, with the recurrence rate in patients who underwent tissue repair being 39.4% and that in patients following prosthetic repair 14.6%. The recurrence rate was significantly influenced by type of repair, obesity, hernia size, wound healing disorders and some chronic comorbidities. We conclude that it is necessary to become familiar with the risk factors for recurrence of incisional hernia in order to eliminate or decrease their effect on the positive outcome of incisional herniorrhaphy.

Adult↗
PubMed1999

Toxicity of major histocompatibility complex class II specific monoclonal antibodies: audietur et altera pars.

AIM: To investigate whether in vivo toxicity of class II major histocompatibility complex (MHC) specific monoclonal antibodies (mAb) is contributed by mAb's constant region binding to Fc receptor (FcR). METHODS: Laboratory mice were injected intravenously (i.v.) with class II MHC-specific mAb of various isotypes and respective antigen-binding fragments, and their clinical status was observed subsequently. RESULTS: All anti-class II mAb of the IgG2a isotype exhibit acute toxicity, manifested in severe lethargy and a frequent death. No adverse effects were observed after the FcR-binding capability of the toxic mAb was eliminated via deletion or mutation of its Fc segment. CONCLUSION: In vivo toxicity of anti-class II mAb appears to be the consequence of the crosslinking of class II+ cells with cells expressing FcR.

Animals↗
PubMed1998

Selective apoptosis of neoplastic cells by the HLA-DR-specific monoclonal antibody.

The human major histocompatibility complex (MHC) class II molecule-specific monoclonal antibody (mAb) 8D1 can induce apoptosis of tumor cells expressing HLA-DR molecules on their surface. This effect is associated with a cross-linking of HLA-DR, since monovalent Fab fragments of 8D1 cannot mediate cytotoxicity unless they are anchored to a solid support. Anti-neoplastic activity of 8D1 is highly selective, i.e. the mAb affects neither the viability nor the function of non-malignant HLA-DR+ cells. These findings raise the possibility of a selective antibody-based anti-tumor therapy of class II positive blood cell neoplasm.

Animals↗
PubMed1998

Peptide dependence of major histocompatibility complex class II specific alloreactive responses.

Splenic cells from transgenic mice, in which a single peptide is complexed to all major histocompatibility complex (MHC) class II molecules, are found to be incapable of triggering primary allogeneic mixed lymphocyte/leucocyte reactions (MLR) when co-cultured with lymphocytes from MHC class II congenic mouse strains. In addition, a single HLA-DR-blocking peptide can completely abrogate the capacity of splenocytes from chimeric HLA-DR/H2-E transgenic mice to stimulate primary MLR of T cells from wild-type mice. These results indicate that the primary alloreactive response is directed against a multitude of peptides presented by allogeneic MHC molecules.

Amino Acid Sequence↗
PubMed1997

The helper T-cell repertoire of mice expressing class II major histocompatibility complex beta chains in the absence of alpha chains.

Mutant mice generated by disrupting the H2-Aab major histocompatibility complex (Mhc) gene are demonstrated here to express Abetab chains in the absence of alpha chains. These mice possess a CD4(+) helper T cell (Th) repertoire that uses predominantly the Vbeta7 T-cell antigen receptor (Tcr) segment for recognition of any protein antigen presented by the alpha-free Abeta molecule. As an alloantigen, the Aalpha-free Abeta molecule is recognized very poorly by T cells from a series of class II disparate mouse strains, indicating that it is grossly different from normal alpha/beta heterodimers. Indeed, molecular modeling suggests a beta/beta homodimer arrangement with an altered geometry of the Tcr contact area. Interestingly, the mutant mice exhibit normal alloreactivity, without a restricted Vbeta usage, toward a series of foreign alpha/beta class II heterodimers, although their T cells developed in the absence of such heterodimers. Thus, the complementarity of Tcr to normal alpha/beta heterodimers, and thereby also alloreactivity, appears to be an ontogeny independent (i. e., germline-encoded) feature.

Animals↗
PubMed1997

T cell repertoire: genomic or somatic bias toward recognition of major histocompatibility complex molecules?

The prevailing concept about a major influence of thymic positive selection on shaping the T cell repertoire during ontogeny is confronted with an old idea emphasizing a dominant role for genetic (evolutionary) factors in molding the recognition potential of mature T cells. Our recent results are not readily interpreted without introducing a new version of the old concept, according to which complementarity to the major histocompatibility complex peptide-binding site is a major evolutionary selective pressure on T cell antigen receptor variable genes, with alloreactivity being a reflection of this fact.

Animals↗
PubMed1996

HLA-DR4-IE chimeric class II transgenic, murine class II-deficient mice are susceptible to experimental allergic encephalomyelitis.

To investigate the development of HLA-DR-associated autoimmune diseases, we generated transgenic (Tg) mice with HLA-DRA-IE alpha and HLA-DRB1*0401-IE beta chimeric genes. The transgene-encoded proteins consisted of antigen-binding domains from HLA-DRA and HLA-DRB1*0401 molecules and the remaining domains from the IE(d)-alpha and IE(d)-beta chains. The chimeric molecules showed the same antigen-binding specificity as HLA-DRB1*0401 molecules, and were functional in presenting antigens to T cells. The Tg mice were backcrossed to MHC class II-deficient (IA beta-, IE alpha-) mice to eliminate any effect of endogenous MHC class II genes on the development of autoimmune diseases. As expected, IA alpha beta or IE alpha beta molecules were not expressed in Tg mice. Moreover, cell-surface expression of endogenous IE beta associated with HLA-DRA-IE alpha was not detectable in several Tg mouse lines by flow cytometric analysis. The HLA-DRA-IE alpha/HLA-DRB1*0401-IE beta molecules rescued the development of CD4+ T cells in MHC class II-deficient mice, but T cells expressing V beta 5, V beta 11, and V beta 12 were specifically deleted. Tg mice were immunized with peptides, myelin basic protein (MBP) 87-106 and proteolipid protein (PLP) 175-192, that are considered to be immunodominant epitopes in HLA-DR4 individuals. PLP175-192 provoked a strong proliferative response of lymph node T cells from Tg mice, and caused inflammatory lesions in white matter of the CNS and symptoms of experimental allergic encephalomyelitis (EAE). Immunization with MBP87-106 elicited a very weak proliferative T cell response and caused mild EAE. Non-Tg mice immunized with either PLP175-192 or MBP87-106 did not develop EAE. These results demonstrated that a human MHC class II binding site alone can confer susceptibility to an experimentally induced murine autoimmune disease.

Amino Acid Sequence↗
PubMed1996

Influence of CD26 and integrins on the antigen sensitivity of human memory T cells.

The antigen sensitivity of class II MHC restricted human CD4 T-cell clones is demonstrated to increase gradually with time after restimulation. This is manifested in a requirement of less antigen in culture, as well as decreased numbers of peptide-MHC complexes per APC for T-cell activation, and in an increased resistance to inhibition by class II MHC blockade. The increase in antigen sensitivity is accompanied by increased cell-surface expression of CD26, LFA-1, and VLA-1, whereas the expression of TCR and a series of other cell-surface molecules remains unchanged. Using appropriate monoclonal antibodies, we have shown that CD26 and LFA-1 contribute directly to the increased antigen sensitivity of "late-stage" T-cell clones. The late-memory T-cell phenotype established in this study is shown to occur also among T cells activated in vivo. We suggest that increasing the antigen sensitivity via antigen-nonspecific molecules is a physiologic mechanism for maintaining T-cell memory in face of decreasing antigen concentration, and for ensuring preferential activation of memory T cells upon repeated encounter with antigen.

Antigen Presentation↗
PubMed1995

Self tolerance to T cell receptor V beta sequences.

T cell tolerance to self is achieved by deletion or inactivation of clones recognizing peptides of self proteins presented by major histocompatibility complex molecules. A considerable fraction of self proteins accessible to the immune system is contributed by the system itself, for example, the receptors used for antigen recognition (antibodies and T cell receptors [TCRs]). Thus far, it has remained unclear, whether antigen receptors are subject to self tolerance, or on contrary, engage into network interactions implying immunity rather than tolerance. In this study, we demonstrate self tolerance to synthetic peptides corresponding to the first hypervariable region of the V beta 8.1 and V beta 8.2 TCR proteins. We also show that the tolerogenic synthetic peptide corresponds to a fragment produced by processing of the V beta protein, and conversely, that a V beta peptide not produced by processing is also not subject to self tolerance. Thus, the rules of tolerance seem to apply to antigen receptors, at least to their germline-encoded portions, in a similar fashion as to other self proteins. This finding has important implications for studies of natural and artificially induced immune networks.

Amino Acid Sequence↗
PubMed1995

Down-regulation of class II major histocompatibility complex molecules on antigen presenting cells after interaction with helper T cells.

The recognition of antigenic peptides by CD4+ helper T cells is demonstrated here to result in a dramatic (up to 90%) decrease in expression of major histocompatibility complex (MHC) class II molecules on the surface of antigen-presenting cells (APC). The reduction is selective to the class II isotype presenting the antigen, but if affects both allelic forms of the same isotype in heterozygous APC. The observed MHC down-regulation requires a specific T cell receptor-peptide-class II interaction, a direct contact between T cell and APC, and the involvement of CD2 molecules. These findings have important implications for the regulation of immune response, self tolerance, and autoimmunity.

Alleles↗
PubMed1995

Down-regulation of class II major histocompatibility complex molecules on antigen-presenting cells by antibody fragments.

Certain HLA class II-specific monoclonal antibodies (mAb) cause up to 90% decrease in the cell surface expression of class II molecules. This down-regulation is isotype-specific, i.e. DR-specific mAb do not affect the expression of DP and DQ molecules. However, antibodies binding to one DR allotype down-regulate both allotypes in heterozygous antigen-presenting cells (APC), indicating that the phenomenon is not a direct consequence of ligation. All down-regulating mAb identified recognize the first (peptide binding) domains of class II heterodimers, and strongly inhibit the activation of class II-restricted human T cells in vitro. Conversely, non-down-regulating mAb fail to inhibit T cell activation, and most of them (four out of five) recognize class II second domains. Down-regulating antibodies are cytotoxic for B lymphoblastoid cell lines and for a small proportion of normal activated B cells. Their F(ab')2 fragments mediate both down-regulation and cytotoxicity, whereas the monovalent Fab fragments are not cytotoxic, but retain the down-regulatory and T cell inhibitory properties. These findings raise the possibility of a class II major histocompatibility complex-specific, antibody-based immunosuppressive therapy without cytotoxic side effects.

Amino Acid Sequence↗
PubMed1993

Temperature and surface changes of dentine and cementum induced by CO2 laser exposure.

The thermal effects of a CO2 laser on the external root surface and inside the root canal were studied in vitro by means of computerized infrared (IR) thermography and a digital thermometer. One-hundred-and-eighty tooth roots with single root canals were irradiated internally and externally with laser power set at 0.5, 1, 1.5, 2, 3 and 4 W. The laser was used in two operating modes: pulsed (pulse 0.5 s) and continuous mode with exposure time of 10 s. Under the conditions of this experiment, temperature rises of between 1.5 and 19.1 degrees C at the external root surface and 1.5 and 12 degrees C inside the root canal and horizontally across the sectioned root surface were recorded. The results obtained with IR camera showed a higher temperature on the external root surface than the digital thermometer during and after lasing the root canal. Scanning electron microscope (SEM) analysis revealed that even low laser energy significantly damaged the external root cementum surfaces.

Body Temperature↗
PubMed1992

Laser induced molar tooth pulp chamber temperature changes.

Temperature changes in enamel tissue and the pulp chamber under the influence of a CO2 laser were measured by direct methods in vitro. X-ray diffraction analysis revealed alpha-Ca3(PO4), the high-temperature modification of enamel hydroxyapatite, thus indicating that the enamel melting temperature was above 1,000 degrees C in the interaction area of laser (continuous wave, 15 s exposure time, 1 mm spot size) and tissue. Powers of 0.5 and 1 W (continuous wave), 1.5 mm spot size, and 10 s exposure time vaporize and carbonize dentin tissue at the cavity bottom of class I preparation molars. The observed temperature rise of 4 degrees C indicates that thermal injury to the pulp tissue does not occur.

Body Temperature↗
PubMed1991

[Possibility of the application of CO2 laser in the prevention of demineralisation of the enamel].

Tooth enamel laser irradiated under certain conditions previously has been shown to have reduced subsurface demineralizations rate. The teeth were cut vertically in half with a thin diamond disc. One half of each tooth served as a control and the other half was irradiated using the CO2 laser. Laser energy was applied at incisive labial surface (15 W, 0.5 s, spot size 3.5 mm). After irradiation the specimens were coated with wax leaving only the windows 3 x 3 mm on the labial surfaces. After experimental demineralisation with 0.2 M sodium acetate and 0.1 M lactic acid solution for 10 days, dissolved calcium and phosphorus were analyzed in the demineralizating solutions using atomic absorption spectrophotometry and colorimetric method (method described by Lowey), respectively. Ca and P concentrations in demineralizing solutions per unit surface area were lower then the controls.

Dental Enamel↗
PubMed1991

[Composite retention area produced by CO2 laser beam].

Laser effect on enamel is manifested as consequence of temperature changes. Enamel melts, vaporises and a crater, and fissures are formed. Retention surface for anchoring of composite resin was obtained in intact approximal surfaces of premolars with CO2 laser (0.5, 1 and 3 W, sport size 1 and 1.5 mm, 0.2 and 0.5 s). The study results reveal composite and lased enamel interfaces are stronger then composite and inlased enamel (p less than 0.01) but weaker than composite and acid pretreated enamel interface (p less than 0.01).

Acid Etching, Dental↗
PubMed1989

Qa-1 restricted recognition of foreign antigen by a gamma delta T-cell hybridoma.

Distinct T-lymphocyte subsets recognize antigens in conjunction with different classes of major histocompatibility complex (MHC) glycoproteins using the T-cell receptor (TCR), a disulphide-linked heterodimer associated with the CD3 complex on the cell surface. In general, class I and class II MHC products provide a context for the recognition of foreign antigens by CD8+ and CD4+ T cells, respectively. This recognition seems to be largely dependent on alpha beta TCR heterodimers, whereas the function of the second gamma delta TCR, present on a minor subpopulation of cells, is still unknown. In the mouse, the existence of six cell-surface MHC class I products (K, D, L, Qa-1, Qa-2 and Tla) has been firmly established by serological, biochemical and genetic evidence. So far, only the most polymorphic of them, K, D and L ('classical' class I) have been reported as restriction elements for T-cell recognition of foreign antigens. The function of the relatively invariant Qa and Tla molecules remains unknown. We have made a T-helper cell hybridoma clone (DGT3) that recognizes synthetic copolymer poly(Glu50Tyr50) in the context of Qa-1 cell surface product, and has a CD4-CD8- phenotype. Our studies indicate that DGT3 cells express the gamma delta TCR on the cell surface, implicating its role in Qa-1-restricted antigen recognition. This is the first evidence that T cells can recognize foreign antigen in association with self Qa product, confirming that Qa molecules not only topologically, but also functionally, belong to the MHC.

Animals↗