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Biomedical subjects

B Kovacs

Publications and source records attributed to B Kovacs.

At least 19 recordsLinked to original sources
PubMed2006

Change of foveal and perifoveal thickness measured by OCT after phacoemulsification and IOL implantation.

PURPOSE: Cataract surgery is known to elicit postoperative macular oedema owing to its traumatic effect. The aim of the study was to measure the foveal and perifoveal thickness of the retina after uneventful phacoemulsification and posterior chamber intraocular lens (PC-IOL) implantation. METHODS: Retinal thickness values of the foveal and perifoveal (fovea+3.0 mm, fovea+6.0 mm) sectors and the minimum values were measured in a prospective study using optical coherence tomography (OCT) in 71 eyes of 71 patients (34 men, 37 women, mean age: 68.8 years) who underwent cataract surgery. Phacoemulsification and 'in the bag' implantation of a foldable PC-IOL was performed under topical anaesthesia. Data were collected 1 day before the operation, and postoperatively at 1, 7, 30, and 60 days. Contralateral eyes of each patient served as controls. 'Student's t-test' was used for statistical analysis, and P<0.05 value was considered significant. RESULTS: No significant change of the thickness values could be measured 1 day after surgery. However, a significant increase could be detected on the postoperative 7, 30, and 60 days in the perifoveal 3.0 and 6.0 mm sectors either calculated alone or averaged together with the foveal values. The initial (preoperative) average value of 234.1+/-2.6 microm (mean+/-SEM, n=536) in the 6.0 mm perifoveal region increased to 242.5+/-2.6 microm (mean+/-SEM, n=488, P<0.01) 1 week, to 247.7+/-4.6 microm (n=352, P<0.01) 1 month, and to 246.0+/-5.9 microm (n=208, P<0.05) 2 months after surgery, which proved to be significant. However, the relative change of macular thickness was moderate, 3.5, 5.6, and 5.3% at the above periods, respectively. In a subgroup of patients (n=34) minimum 6 months after cataract surgery, the 6.0 mm perifoveal values were found to be elevated at (237.8+/-3.9 microm, mean+/-SEM, n=272) as compared to the control eyes (233.9+/-3.8 microm, mean+/-SEM, n=272). The difference was 1.7% and proved not to be significant (P>0.05). CONCLUSIONS: Mild subclinical perifoveal oedema following cataract surgery was detected using OCT at postoperative day 7 to 6 months. The minimal and the foveal values in itself are inadequate to describe the phenomenon. The macular thickness values of the perifoveal 3.0 and 6.0 mm sectors alone or averaged together with the foveal values provide more accurate description of the postoperative macular oedema.OCT enables the detection of minimal increases in perifoveal retinal thickness even 6 months after cataract surgery.

Aged↗
PubMed2006

The role of biofilm infection in urology.

In the process of endourological development a great variety of foreign bodies have been invented besides urinary catheters on which biofilm can be formed. Bacteria in the biofilm are less sensible to antibiotics. An additional problem of medical biomaterials in the urinary tract environment is the development of encrustation and consecutive obstruction. In this review, we tried to sum up the conditions where biofilm formation has a great impact on the development or maintenance of urological infections and on treatment success. Modification of the biomaterial surface seems to be the most promising prevention strategy for bacterial biofilms. Easier methods for diagnosing and quantifying biofilm infection, to develop more specific antimicrobial agents and ideal device surfaces would surely help the fight against biofilm formation.

Anti-Bacterial Agents↗
PubMed2000

C1 inhibitor prevents capillary leakage after thermal trauma.

OBJECTIVE: In burned patients, activation of the complement and clotting systems is suggested to play an important role in the development of the capillary leak syndrome and inflammatory tissue destruction. In an animal model of thermal trauma, the possible protective effect of C1 inhibitor (C1Inh), a major control protein of both the complement and clotting systems, was investigated. DESIGN: Prospective, controlled study. SETTING: Animal model. SUBJECTS: Healthy pigs weighing 30 kg. INTERVENTIONS: Pigs were scalded for 25 secs with 75 degrees C hot water to achieve a 30% total body surface deep partial-thickness burn. The treatment group (n = 8) received C1Inh concentrate at an initial dose of 100 units/kg body weight immediately after thermal trauma, followed by three further applications every 12 hrs. Two control groups included animals that were either scalded (n = 8) or not scalded (n = 7) and treated with lactated Ringer's solution. MEASUREMENTS: Before and at various time points after trauma blood samples were analyzed for complement activation (APH50, CH50, SC5b-9, C3). Continuous monitoring of hemodynamic variables was performed and postmortem histologic examination of specimens from lung, heart, liver, kidney, stomach, duodenum, jejunum, ileum, and colon was carried out. Aseptically collected mesenteric lymph nodes were pooled and screened for bacterial translocation. For evaluation of the burn wound, biopsies from defined scalded and not scalded areas were taken daily. As a measure for edema formation, the weight of the animals was recorded every 2 hrs. RESULTS: After C1Inh treatment, which led to a significantly reduced complement activation, the clinical outcome was clearly improved, as indicated by vital signs and as demonstrated by reduced edema formation. Treated animals presented a diminished bacterial translocation. Pathologic alterations were clearly diminished in the burned skin, in shock-related organs, and in the intestines. CONCLUSION: Application of C1Inh appears to be an effective means to prevent capillary leakage and inflammatory tissue destruction after thermal trauma.

Animals↗
PubMed2000

Transverse myelopathy in systemic lupus erythematosus: an analysis of 14 cases and review of the literature.

OBJECTIVE: To give a comprehensive review of transverse myelopathy (TM), a rare but serious condition reported in 1-2% of patients with systemic lupus erythematosus (SLE). METHODS: 14 patients with SLE and TM were evaluated and 91 additional cases published in the English and German literature reviewed. RESULTS: TM presented either as the initial manifestation or within five years of the diagnosis of SLE. Most patients presented with a detectable sensory deficit at the thoracic level. In our 14 patients, 22% of the patients showed complete neurological recovery, whereas in the total patient population of 105 (our cases plus those reviewed in the literature), complete recovery was observed in 50%, partial recovery in 29% and no improvement or deterioration in 21%. Treatment with intravenous methylprednisolone followed by cyclophosphamide seemed to be most effective. Seventy per cent of the total patient population had abnormal magnetic resonance imaging findings. In our group of 14 patients, those with higher disease activity (measured by the SLAM) at onset of TM were treated more aggressively (for example, with plasmapheresis and intravenous pulse cyclophosphamide). TM in our patients was associated with antiphospholipid antibodies in 43% of the cases as compared with 64% of the total patient population. Optic neuritis occurred in 48% of the total patient population with SLE and TM, suggesting an association. CONCLUSIONS: TM in SLE is a poorly understood entity. Outcome might be more favourable than previously suggested. There is an association of TM with antiphospholipid antibodies in SLE patients. Treatment including intravenous cyclophosphamide may improve the final outcome. This report emphasises the need for multicentre trials to establish guidelines for optimal treatment.

Adult↗
PubMed1999

End-stage renal disease in sarcoidosis of the kidney

We describe two cases of black women with biopsy-proven sarcoidosis of the kidney who developed end-stage renal disease. Treatment with high-dose glucocorticoids resulted in a good initial response, followed by progressive deterioration of renal function requiring hemodialysis.

Journal Article↗
PubMed1999

Crosslinking of Fas/CD95 suppresses the CD3-mediated signaling events in Jurkat T cells by inhibiting the association of the T-cell receptor zeta chain with src-protein tyrosine kinases and ZAP70.

Crosslinking of Fas (APO-1/CD95) on the surface of T cells initiates a biochemical cascade leading to programmed cell death. We have previously shown that crosslinking of Fas with an apoptosis-inducing IgM anti-Fas mAb results in suppression of the CD3-initiated cell signaling including Ca2+ mobilization and protein tyrosine phosphorylation. We conducted experiments to decipher the mechanisms whereby the cross talk between the Fas- and CD3 signaling pathways occur. We used lysates from Jurkat T and examined the composition of the TCR zeta chain-precipitated immune complexes using immunoblots. While crosslinking of Fas affected the association of p59fyn and p56lck tyrosine kinases with the TCR zeta chain to a limited degree, it dramatically inhibited the association of the protein tyrosine kinase ZAP70 with the zeta chain. In cells that were preincubated with an apoptosis-inducing anti-Fas mAb, the binding of the protein tyrosine phosphatases SHP-1 to the TCR zeta chain was increased. These experiments indicate that crosslinking of Fas interferes with early T cell signaling events by promoting the recruitment of SHP-1 and decreasing the association of protein tyrosine kinases with TCR zeta chain. Therefore, crosslinking of Fas antigen may regulate the antigen-induced T cell response and play an active role in the T cell anergy.

Journal Article↗
PubMed1997

Detection of hyperdiploid malignant cells in body cavity effusions by fluoresence in situ hybridization on ThinPrep slides.

BACKGROUND: Benign body cavity effusions sometimes cannot be distinguished from malignant ones by conventional cytology. The authors performed fluorescence in situ hybridization (FISH) on ThinPrep slides using chromosome specific probes to see if hyperdiploid malignant cells could be detected in 20 body cavity effusions. The results were then compared with those of conventional cytology. METHODS: A total of 20 body cavity effusions from 19 patients were studied using conventional cytology and FISH. Probes specific for chromosomes 3, 8, 10, and 12 were used to detect hyperdiploidy on ThinPrep slides (Cytyc Corporation, Boxborough, MA). RESULTS: A total of 13 patients had malignant conditions (either prior history of malignancy or the presence of malignancy anywhere in the body). Conventional cytology and FISH were both positive in 5 of these patients (6 samples) and negative in 2 patients. The results for one sample were inconclusive by both methods. There were 5 discrepant cytology-FISH results in patients with malignant conditions. One sample was positive by FISH and negative by cytology, one was positive by FISH and "atypical" by cytology, and three were inconclusive by FISH and negative by cytology. FISH results were either negative (in 4 samples) or inconclusive (in 2 samples) in the 6 patients with benign conditions. CONCLUSIONS: FISH can detect hyperdiploid malignant cells in body cavity effusions and is especially useful when the major cell population consists of malignant cells that cannot be differentiated from mesothelial or "atypical" cells. It is less useful in detecting a small population of malignant cells hidden in an inflammatory or reactive cell background. More studies are needed to establish diagnostic criteria further and to assess the clinical usefulness of this procedure.

Adult↗
PubMed1997

Lymphocytes, cytokines, inflammation, and immune trafficking.

Studies reported during the past year have added new knowledge to our understanding of the pathogenesis of systemic lupus erythematosus. A study of sibpairs with lupus revealed a strong linkage of a region located at chromosome 1q41-42 that crossed ethnic barriers. B-cell receptor-initiated signaling events, such as tyrosine protein phosphorylation and intracellular calcium concentrations, were found to be increased in patients with lupus in a disease- and clinical activity-independent manner. T cells from patients with lupus express increased amounts of the CD40 ligand, which is functional because it helps B cells to produce anti-DNA antibodies and express more CD80 (B7-1) on their surface. Only occasionally do lupus patients display structural defects of either Fas antigen or ligand molecules, and although spontaneous apoptosis is increased in lupus cells (as well as in other systemic autoimmune disorders), the activation-induced T-cell death is defective.

Animals↗
PubMed1997

Increased expression of functional Fas-ligand in activated T cells from patients with systemic lupus erythematosus.

The Fas ligand induces apoptosis upon binding to Fas/APO-1 (CD95) bearing target cells. Activation induced cell death (AICD) in T cells is mediated by upregulation of Fas ligand on the cell surface membrane upon crosslinking of the TCR. AICD is considered to be essential for the elimination of autoreactive T cells in the peripheral blood. To elucidate possible abnormalities in the process of AICD in human SLE, we studied the expression and function of Fas ligand in polyclonal T cell lines from patients with SLE, patients with other rheumatic diseases and normal controls. SLE T cells expressed on their surface significantly higher amounts of Fas ligand compared to the two control groups. Stimulation of the cells with anti-CD3 mAb lead to further increase in surface membrane Fas ligand expression in all three groups with SLE expressing the highest amounts. The percentage of increase was though lower in SLE T cells than in normal T cells or disease control cells. The T cells were examined for Fas ligand-mediated cytotoxicity in a 51Cr release assay using Fas-expressing normal T cells as target cells. There was no difference in SLE and control T cells with regard to specific 51Cr lysis, indicating that the Fas ligand expressed by the SLE T cells is functional. Our data show that activated T cells from patients with SLE express high amounts of functional Fas ligand with intact TCR-mediated upregulation. This could account for the high apoptotic rates that have been observed in lymphocytes from patients with SLE.

Adult↗
PubMed1996

B cells from patients with systemic lupus erythematosus display abnormal antigen receptor-mediated early signal transduction events.

To understand the molecular mechanisms that are responsible for the B cell overactivity that is observed in patients with SLE, we have conducted experiments in which the surface immunoglobulin (sIg)-mediated early cell signaling events were studied. The anti-sIgM-mediated free intracytoplasmic calcium ([Ca2+]i) responses were significantly higher in SLE B cells compared with responses of normal individuals and to those of patients with other systemic autoimmune rheumatic diseases. The anti-IgD mAb induced [Ca2+]i responses were also higher in lupus B cells than in controls. The magnitude of anti-sIgM-mediated Ca2+ release from intracellular stores was also increased in B cells from SLE patients compared with normal controls. The amount of inositol phosphate metabolites produced upon crosslinking of sIgM was slightly higher in patients with lupus than in normal controls, although the difference was not statistically significant. In contrast, the degree of anti-sIgM-induced protein tyrosine phosphorylation was obviously increased in lupus patients. Our study demonstrates clearly for the first time that SLE B cells exhibit aberrant early signal transduction events, including augmented calcium responses after crosslinking of the B cell receptor and increased antigen-receptor-mediated phosphorylation of protein tyrosine residues. Because the above abnormalities did not correlate with disease activity or treatment status, we propose that they may have pathogenic significance.

Adult↗
PubMed1996

Defective antigen-presenting cell function in patients with systemic lupus erythematosus.

OBJECTIVE: Patients with systemic lupus erythematosus (SLE) who exhibit defective in vitro responses to recall antigens and normal responses to alloantigens have been shown to have an abnormality in antigen-presenting cell (APC) function. This study was undertaken to further characterize this defect in APC function in lupus patients. METHODS: Mononuclear cells (MNC) from the peripheral blood of patients with SLE and from normal individuals were cultured in the presence of either recall antigen tetanus toxoid (TT), anti-CD3 (OKT3) monoclonal antibody, or alloantigens, and proliferative or interleukin-2 responses were assessed. Cell surface expression of B7-1 was assessed by flow cytometry. RESULTS: MNC from all normal individuals and from 7 patients with SLE responded to both TT and alloantigen and were designated +/+. Twelve SLE patients did not respond to TT but did respond to alloantigen stimulation and were designated -/+. In both normal subjects and SLE patients, the ability to respond to OKT3 correlated strongly with the ability to respond to recall antigen. A defect in APC costimulatory function was suggested by data demonstrating that interferon-gamma-induced expression of B7-1 was significantly reduced in SLE patients compared with controls. Neither controls nor SLE patients expressed detectable amounts of surface B7-1 molecule on resting APC. Defective recall and anti-CD3-stimulated responses could be enhanced in SLE patients in the presence of B7/BBl-transfected P815 murine mastocytoma cells underscoring an SLE-associated defect in costimulatory activity. However, nontransfected P815 cells were also able to enhance responses to OKT3 in -/+ patients; blocking experiments showed that this was mediated through an IgG Fc receptor-dependent mechanism. CONCLUSION: These data indicate that SLE-associated defects in APC function in vitro can be accounted for by abnormalities in APC surface membrane molecules such as B7, IgG Fc receptors, and possibly others.

Adolescent↗
PubMed1996

Defective CD3-mediated cell death in activated T cells from patients with systemic lupus erythematosus: role of decreased intracellular TNF-alpha.

Activation-induced cell death (AICD) plays an important role in the regulation of the immune response by eliminating preactivated and potentially autoreactive cells. To elucidate possible abnormalities of AICD in human systemic lupus erythematosus (SLE), we studied AICD in activated T cells from patients with SLE and normal controls. CD3-mediated cell death was determined in short-term T cell lines by flow cytometry using propidium iodide staining and analysis of DNA subdiploid peak populations. It was found to be significantly lower in T cells from SLE patients compared to cells from normal controls. Anti-Fas mAb-mediated cell death was similar in SLE and control cell lines. CD3-mediated AICD could be blocked in control and SLE T cell lines by an IgG anti-Fas mAb. Indirect immunofluorescence analysis showed statistically significantly less intracellular TNF-alpha in SLE T cells than in control cells. These data show that activated T cells from patients with SLE are relatively resistant to a TCR-mediated death stimulus although they display intact anti-Fas mAb-mediated cell death. Defective antigen-mediated cell death can contribute to increased numbers of activated autoreactive cells in lupus patients.

Adolescent↗
PubMed1995

Cross-linking of the Fas/APO-1 antigen suppresses the CD3-mediated signal transduction events in human T lymphocytes.

The Fas/APO-1 Ag, a member of the TNF-R family, mediates apoptosis (programmed cell death, PCD). PCD has been recognized to be important in the regulation of normal and autoimmune responses. However, the underlying molecular mechanisms are not fully known. To elucidate the role of the Fas Ag in lymphocyte activation, we investigated the influence of Fas Ag cross-linking on CD3/TCR-mediated signal transduction in IL-2-dependent human T cell lines. Early signal transduction events were evaluated in 10-day-old T cell lines using anti-Fas and anti-CD3 mAbs. Incubation of Indo-1-loaded cells with anti-Fas mAb (10 micrograms/ml), but not with an isotypic control mAb almost completely inhibited the anti-CD3-mediated Ca2+ influx. This inhibition was mAb concentration dependent and was detected after incubation for at least 15 min. Cross-linking of the Fas Ag did not affect the anti-CD3-mediated release of Ca2+ from the internal stores or the thapsigargin-mediated Ca2+ influx. Anti-Fas mAb-incubated cells also showed decreased CD3-mediated inositol 1,4,5-trisphosphate production. Preincubation of cells with anti-Fas mAb inhibited the anti-CD3-mediated tyrosine phosphorylation of multiple cellular proteins. Cross-linking of the Fas Ag for up to 6 h did not alter the expression of CD3 on the surface of the T cells. Preincubation of Indo-1-loaded EBV-transformed B cells with anti-Fas mAb did not affect the anti-mu Ab-induced increase in intracellular calcium ([Ca2+]i). Our results show that cross-linking of the Fas Ag can suppress the receptor-mediated signaling process in human T but not B cells.

Antibodies, Monoclonal↗
PubMed1995

TCR/CD3 complex-mediated signal transduction pathway in T cells and T cell lines from patients with systemic lupus erythematosus.

We studied the TCR/CD3 complex-mediated signal transduction pathway in freshly isolated T cells and T cell lines from patients with systemic lupus erythematosus (SLE). The peak and 5-min anti-CD3 mAb-mediated free intracytoplasmic Ca2+ concentration ([Ca2+]i) increase was statistically significant higher in fresh T cells from SLE patients than in control T cells. Increased CD3-mediated [Ca2+]i responses were observed in T cells from patients with SLE but not in T cells from other rheumatic diseases. Furthermore, significantly increased CD3-mediated [Ca2+]i responses were observed in T cell lines from SLE patients but not from controls. Although the [Ca2+]i response did not correlate with the global SLE disease activity or individual clinical manifestations, it was significantly higher in the group of patients who were not on treatment. Both CD4+ and CD8+ T cell subsets from peripheral blood cells and T cell lines displayed higher CD3-mediated [Ca2+]i responses than their normal counterparts. The peak of the response occurred earlier in the patient than in the normal group. The amount of Ca2+ that was released from the intracellular stores was higher in lupus than control T cells. The TCR/CD3-induced production of inositol phosphate metabolites in SLE cells was comparable with controls. The sarcoplasmic and endoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin-induced [Ca2+]i response was similar in both SLE and normal T cells. Our experiments demonstrate for the first time a definite abnormality in the early steps of the TCR/CD3-mediated signal transduction pathway in T cells from SLE patients that involves increased release of Ca2+ from intracellular stores.

Adolescent↗
PubMed1993

Extracorporeal circulation: in vivo and in vitro analysis of complement activation by heparin-bonded surfaces.

Complement activation was analyzed during extracorporeal CO2 removal to compare heparin-coated with standard surfaces where systemic heparinization was required. In vivo studies were performed in adult sheep for up to 5 days under standardized conditions using a capillary membrane oxygenator. Applying assays for hemolytic complement function (CH50, APH50) and C3-derived split products, we found that complement activation was markedly reduced in sheep connected to an extracorporeal circuit where heparin was covalently bound by end-point attachment. In addition, incubation of human serum in a miniaturized circulation system revealed less complement activation by heparin-bonded surfaces, as evaluated by enzyme-linked immunosorbent assays for C3a and the activation-specific protein-protein complexes, C1rsC1 inhibitor (classical pathway) and C3b(Bb)P (alternative pathway). Our results provide further evidence that biocompatibility can be improved by end-point attachment of heparin to the surfaces of the extracorporeal circuit.

Animals↗
PubMed1992

[Importance of diagnosis in facial pain].

The diagnosis and treatment of facial pain remains a great challenge for oral and maxillofacial surgeons. By taking an exact anamnesis--especially a pain anamnesis--and by starting specific examinations the patient can quickly be recommended to a qualified therapist. The pain syndromes are classified according to the IASP (International Association for the Study of Pain). The pain syndromes the maxillofacial surgeon is most frequently confronted with--idiopathic trigeminal neuralgia, atypical facial pain and the temporomandibular joint--are described. The necessity of a multidisciplinary examination is emphasized and the different diagnostic investigations are illustrated, particularly in the case of myo-arthropathy. Beside the analysis of temporomandibular joint dysfunction, a radiologic examination is performed. In some cases the advise of a neurologist, ophthalmologist or otolaryngologist may be indicated.

Adult↗
PubMed1992

[Treatment concept of facial pain].

The therapy of chronic facial pain still poses an important challenge. A therapeutical scheme in four steps has been developed. This scheme enables modification of the pain therapy depending on localisation, intensity and former treatment. It consists of the following steps: 1. Transcutaneous electrical nerve stimulation. 2. Medication 3. Extracranial glycerol blocking of the trigeminal nerve 4. Neurosurgical treatment with thermocoagulation, chemical glycerol-rhizotomy and microsurgical decompression. The different therapeutical steps have no influence on each other.

Antipsychotic Agents↗