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Biomedical subjects

B Moser

Publications and source records attributed to B Moser.

At least 19 recordsLinked to original sources
PubMed2006

Recovery from giant cell myocarditis with ECMO support and utilisation of polyclonal antithymocyte globulin: a case report.

Giant cell myocarditis (GCM) is a rare and frequently fatal disorder. Patients suffer of ventricular arrhythmias or congestive heart failure. Here we describe a patient with cardiogenic shock and histological verified GCM. The patient was saved by implantation of extracorporeal membrane oxygeneation (ECMO) device and concomitant application of Rabbit antithymocyte globuline (rATG, Thymoglobulin, Sangstat), cyclosporine, and steroids in the acute event. 12 months after the crisis the patient evidences NYHA class I heart function and only a moderate impairment of heart function (EF 55%). The novel utilisation of ECMO in GCM related cardiogenic shock and application of rATG have prooven life-saving in this patient. Studies utilizing rATG in the treatment of GCM are warrented.

Antilymphocyte Serum↗
PubMed2006

Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells.

BACKGROUND: Multiple studies have demonstrated a link between periodontal infections and vascular disease. Porphyromonas gingivalis, a major periodontal pathogen, has been shown to adhere to and invade endothelial cells. OBJECTIVE: In order to dissect mechanisms underlying these observations, we assessed the role of P. gingivalis infection in modulating properties of endothelial cells linked to atherothrombosis. METHODS: Primary human aortic endothelial cells (HAEC) were infected with either P. gingivalis 381 or its non-invasive fimbriae-deficient mutant, DPG3. Markers of coagulation and thrombosis were assessed 8 h and 18 h postinfection in cell lysates and supernatants. RESULTS: Infection with P. gingivalis 381 significantly enhanced tissue factor expression and activity, and suppressed levels of tissue factor pathway inhibitor. Furthermore, P. gingivalis infection decreased levels and activity of tissue plasminogen activator, and enhanced plasminogen activator inhibitor-1 antigen and activity. Consistent with an important role for bacterial adhesion/invasion in this setting, infection with DPG3 failed to induce procoagulant properties in HAEC. Most of the above effects of P. gingivalis 381 were more apparent at the later time point (18 h postinfection). This suggests that P. gingivalis infection, rather than having an immediate and direct effect, might activate pathways that, in turn, trigger endothelial procoagulant mechanisms. CONCLUSIONS: Taken together these data demonstrate for the first time that infection with a periodontal pathogen induces procoagulant responses in HAEC.

Aorta↗
PubMed2005

[Analgesia with remifentanil in spontaneously breathing patients undergoing brief but painful radiological procedures].

INTRODUCTION: Percutaneous transhepatic biliary drainage (PTBD) and stenting are very painful procedures in interventional radiology and require potent analgesia; employing remifentanil in spontaneously breathing patients may be one possible strategy. PATIENTS AND METHODS: The study group was composed of 18 men and 2 women with a mean age of 63+/-10 (mean+/-SD) years. Pain intensity was measured with a VAS score before the procedure, after local anesthesia on the rib cage, after stenting and after the radiology procedure. RESULTS: Remifentanil infusion (dosage: 0.12-0.30 microg/kg body weight/min) was infused throughout the entire radiology procedure according to physical status, past medical history, individual pain, and clinical assessment. During insufflation of 10l O(2)/min via a venturi mask, oxygen saturation did not fall below 96% at any time-point during the procedure. In the VAS score, we noted a decrease after starting the remifentanil infusion towards the end of procedure. All patients were able to move into bed without help. Postoperatively, no analgesics and no antiemetics were needed. CONCLUSIONS: Employing a remifentanil infusion for brief interventional radiology procedures in palliative treatment of patients resulted in high patient and radiologist comfort.

Adult↗
PubMed2005

One night in a snowbank: a case report of severe hypothermia and cardiac arrest.

Hypothermia < 28 degrees C is rarely compatible with life, with only a few cases described surviving such low temperatures. We present a case of a man who survived with a core body temperature below 21.0 degrees C after spending a night in a snowbank with an ambient temperatures as low as -20.0 degrees C. Prolonged CPR and early initiation of extracorporeal membrane oxygenation enabled survival without neurological deficit at hospital discharge. Frostbite was limited to both hands and all toes only; although the entire upper and lower extremity appeared to be deeply frozen on admission, amputation of both hands was inevitable and resulted in permanent disability.

Amputation, Surgical↗
PubMed2005

Alpha-Gal on bioprostheses: xenograft immune response in cardiac surgery.

BACKGROUND: The alpha-Gal (Galalpha1,3-Galbeta1-4GlcNAc-R) epitope is the major xenoantigen causing hyperacute rejection of pig organs transplanted into primates. Porcine bioprostheses are utilized in cardiac surgery. However, premature degeneration of bioprostheses has limited utilization in younger patients and the immune response remains elusive. We sought to investigate whether a specific alpha-Gal immune response may play a role in this clinical scenario. MATERIALS AND METHODS: We investigated the presence of alpha-Gal-epitope on native and fixed porcine valves by means of confocal laser scanning microscope (CLSM). ELISA was utilized to evidence whether implantation of bioprostheses elicits augmentation of pre-existing cytotoxic anti alpha-Gal IgM antibodies within 10 days of surgery. Patients who underwent coronary artery bypass grafting (CABG) or mechanical valve replacement served as controls (each group, n = 12). To corroborate the clinical relevance of the alpha-Gal immune response in vivo, we studied serum obtained before and after implantation of bioprostheses and its potency to lyse porcine alpha-Gal-bearing PK15 cells. RESULTS: We found the immunogenic alpha-Gal-epitope on fibrocytes interspersed in the connective tissue of porcine valves as determined by vimentin/IB4 lectin binding. Moreover, patients who were provided with a bioprostheses had developed a significant increase of naturally occurring cytotoxic IgM antibodies directed towards alpha-Gal after surgical intervention as compared with control patients (P < 0.0001, respectively). Sera obtained from the patients after the implantation of bioprostheses demonstrated an increased cytotoxicity against alpha-Gal-bearing PK-15 cells as compared with preoperative sera (P < 0.001). The specificity of the cytotoxic effects was proven as soluble Galalpha1-3Galbeta1-4GlcNAc markedly inhibited cell death of alpha-Gal-bearing PK15 cells (P < 0.001). CONCLUSION: Our data suggest that implantation of bioprostheses in cardiac surgery induces a xenograft-specific immune response. Procedures diminishing the presence of alpha-Gal on bioprostheses, such as utilization of genetically manipulated alpha-Gal-deficient xenograft or pretreatment with alpha-Galactosidase, might diminuate the immune response against bioprostheses and extend durability.

Animals↗
PubMed2005

Heightened levels of circulating 20S proteasome in critically ill patients.

BACKGROUND: Recently, circulating proteasome core particles (20S proteasome) have been suggested as a marker of cell damage and immunological activity in autoimmune diseases. Aberrant leucocyte activation and increased lymphocyte apoptosis with consecutive T-cell unresponsiveness is deemed to play a pivotal role in the sepsis syndrome. Moreover sepsis-induced muscle proteolysis mainly reflects ubiqutin proteasome-dependent protein degradation. We therefore sought to investigate serum levels of 20S proteasome in critical ill patients. MATERIAL AND METHODS: Case-control-study at a university hospital intensive care unit; 15 patients recruited within 24-48 h of diagnosis of sepsis, 13 trauma patients recruited within 24 h of admission to the ICU, a control group of 15 patients who underwent abdominal surgery, and 15 healthy volunteers. ELISA was used to measure the concentration of 20S proteasome in the sera of the patients and controls. Data are given as mean +/- SEM. Mann-Whitney U-test was used to calculate significance and a P-value of 0.05 was considered to be statistically significant. RESULTS: Marked increase of 20S proteasome was detected in the sera of septic patients (33 551 +/- 10 034 ng mL-1) as well as in trauma patients (29 669 +/- 5750 ng mL-1). In contrast, significantly lower concentrations were found in the abdominal surgery group (4661 +/- 1767 ng mL-1) and in the healthy control population (2157 +/- 273 ng mL-1). CONCLUSION: Detection of 20S proteasome may represent a novel marker of immunological activity and muscle degradation in sepsis and trauma patients, and may be useful in monitoring the clinical effect of proteasome-inhibitors.

Adult↗
PubMed2004

Chemokines: role in inflammation and immune surveillance.

Chemotactic migration of leucocytes largely depends on adhesive interaction with the substratum and recognition of a chemoattractant gradient. Both aspects, cell adhesion and chemotaxis, are regulated by members of the family of chemotactic cytokines (chemokines) comprising structurally related and secreted proteins of 67-127 amino acids in length. Breakdown in the control of leucocyte mobilisation contributes to chronic inflammatory diseases and, hence, interference with chemokine function is a promising approach for the development of novel anti-inflammatory medication. Chemokines target all types of leucocyte, including haematopoietic precursors, mature leucocytes of the innate immune system as well as naive, memory, and effector lymphocytes. The combinatorial diversity in responsiveness to chemokines ensures proper tissue distribution of distinct leucocyte subsets under normal and inflammatory/pathological conditions. Here, we discuss recent views on the role of chemokines in controlling tissue localisation of human memory T cells under steady state (non-inflamed) conditions. Emphasis is placed on a concept describing distinct subsets of memory T cells according to their primary residence in peripheral blood, secondary lymphoid tissues, or peripheral (extralymphoid) tissues.

Chemokines↗
PubMed2004

Increased serum concentrations of soluble CD95/Fas and caspase 1/ICE in patients with acute angina.

OBJECTIVES: To investigate the expression of death inducing receptors in the sera of patients with stable and unstable angina. DESIGN: 80 consecutive patients with stable (n = 40) or unstable (n = 40) angina pectoris were studied. Serum concentrations of soluble CD95 (sCD95), soluble CD95 ligand (sCD95L; CD178), tumour necrosis factor (TNF) alpha, soluble TNFalpha receptor type 1 (sTNFR1), and interleukin 1beta converting enzyme (ICE; caspase 1) were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: Significant increases in the concentrations of sCD95 and ICE (p < 0.001 and p < 0.023, respectively) were found in the serum from patients with unstable angina relative to those with stable angina. There were no significant differences in the concentrations of sCD95L, TNF alpha, and sTNFR1 between the groups. CONCLUSIONS: These data provide the first evidence that sCD95 and ICE are important serological markers that may help to discriminate between stable and unstable angina. This observation may warrant further clinical study to elucidate the clinical impact of sCD95 and ICE in acute coronary syndromes.

Acute Disease↗
PubMed2003

Rapamycin as rescue therapy in a patient supported by biventricular assist device to heart transplantation with consecutive ongoing rejection.

Rapamycin is a new immunosuppressive agent that has been shown to be effective in acute heart allograft rejection. This case documents a patient suffering from cardiac sarcoidosis who was bridged to transplantation for 90 days with ongoing rejection after allograft implantation. Rejection did not abate despite treatment with antithymocyte globulin (ATG), FK506, a mycophenolate switch and courses of multiple apheresis. Initiation of rapamycin treatment resulted in a rapid resolution of cardiac rejection and reduction of concomitant immunosuppressive agents with few side-effects. Most notably was the reduction of panel reactive antibodies within a few weeks after the rapamycin initiation. This case illustrates that the utilization of rapamycin ceased ongoing rejection in a patient with a clear hyperimmune state despite prior extensive utilization of a variety of immunosuppressive strategies after heart transplantation.

Adult↗
PubMed2003

Transmitted light microscopy of a fibre reinforced metal.

A method is presented for studying fibre damage in continuous fibre reinforced composites. It is based on contrasting the transmission of light through intact translucent fibres with the light through fractured or dead-ended fibres. The method is applied in order to detect processing-induced fibre fractures in aluminium reinforced with continuous alumina fibres.

Journal Article↗
PubMed2002

RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response.

The receptor for advanced glycation end products (RAGE) and its proinflammatory S100/calgranulin ligands are enriched in joints of subjects with rheumatoid arthritis (RA) and amplify the immune/inflammatory response. In a model of inflammatory arthritis, blockade of RAGE in mice immunized and challenged with bovine type II collagen suppressed clinical and histologic evidence of arthritis, in parallel with diminished levels of TNF-alpha, IL-6, and matrix metalloproteinases (MMP) 3, 9 and 13 in affected tissues. Allelic variation within key domains of RAGE may influence these proinflammatory mechanisms, thereby predisposing individuals to heightened inflammatory responses. A polymorphism of the RAGE gene within the ligand-binding domain of the receptor has been identified, consisting of a glycine to serine change at position 82. Cells bearing the RAGE 82S allele displayed enhanced binding and cytokine/MMP generation following ligation by a prototypic S100/calgranulin compared with cells expressing the RAGE 82G allele. In human subjects, a case-control study demonstrated an increased prevalence of the 82S allele in patients with RA compared with control subjects. These data suggest that RAGE 82S upregulates the inflammatory response upon engagement of S100/calgranulins, and, thereby, may contribute to enhanced proinflammatory mechanisms in immune/inflammatory diseases.

Alleles↗
PubMed2002

Death-inducing receptors and apoptotic changes in lymphocytes of patients with heart transplant vasculopathy.

The specific role of lymphocyte apoptosis and transplant-associated atherosclerosis is not well understood. The aim of our study was to investigate the impact of T cell apoptotic pathways in patients with heart transplant vasculopathy. Amongst 40 patients with cardiac heart failure class IV who have undergone heart transplantation, 20 recipients with transplant-associated coronary artery disease (TACAD) and 20 with non-TACAD were investigated one year postoperative. Expression of CD95 and CD45RO, and annexin V binding were measured by FACS. Soluble CD95, sCD95 ligand (sCD95L), tumour necrosis factor receptor type 1 (sTNFR1), and histones were measured in the sera by ELISA. The percentage of cells expressing CD3 and CD4 was significantly reduced in TACAD as well as in non-TACAD patients as compared with control volunteers. Interestingly, the proportion of CD19+ (B cells) and CD56+ (NK) cells was increased in TACAD groups (versus non-TACAD; P < 0.01, and P < 0.001, respectively). In contrast to sCD95, the expression of CD95 (APO-1/Fas) and CD45RO (memory T cells), and sCD95L were significantly increased in non-TACAD and TACAD patients. T cell activation via CD95 with consecutive apoptosis was increased in both groups. The concentration of sTNFR1, IL-10 and histones was significantly elevated in sera from TACAD than non-TACAD patients, and in both groups than in healthy controls. These observations indicate that the allograft may induce a pronounced susceptibility of CD4+ T cells to undergo apoptosis and antibody-driven activation-induced cell death. This data may suggest a paradox immune response similar to that seen in patients with autoimmune diseases.

Aged↗
PubMed2002

Activation-induced T cell death, and aberrant T cell activation via TNFR1 and CD95-CD95 ligand pathway in stable cardiac transplant recipients.

Specific blockade by antibodies (Abs) utilized in induction therapy may cause activation-induced cell death (AICD) in lymphocytes of transplant recipients, preactivated via CD95 and tumour necrosis factor-alpha receptor type 1 (TNFR1), and reduce allograft rejection frequency. Amongst 618 heart transplant (HTX) patients receiving antithymocytes globulin (ATG) therapy, 14 recipients with IVUS-verified freedom of transplant vasculopathy were studied. The control group contained 14 patients awaiting transplantation, classified by the New York Hearth Association heart failure as class IV. From 618 HTX patients 89% were free of rejection grade ISHLT > or =2-3 within 3-month post transplantation and 86% after one year. The death inducing receptors (DIR) such as CD95, CD95L and soluble TNFR1 were significantly increased in HTX recipients versus controls, as demonstrated by FACS, immunoblotting or ELISA (P < 0.001). The presence of increased DIR and in vivo apoptosis in HTX recipients, indicated by annexin-V binding, was further confirmed by the presence of high concentration of histones in the sera of patients. ATG, anti-IL-2R and OKT-3 Abs inhibited cell proliferation in a dose-dependent manner. The induction of apoptosis and/or necrosis was demonstrated in cells cultured with these Abs by annexin-V and 7-aminoactinomycin staining, respectively. Our findings demonstrate that T cells from HTX recipients express high level of CD95, CD95L and soluble TNFR1, and undergo apoptosis and AICD. These cells recognizing donor alloantigens may be selectively eliminated in vivo, and should be responsible for the observed immunological unresponsiveness, indicated by low rejection rates in our patient cohort treated by conventional triple therapy.

Adult↗