Biomedical subjects

Martin Scholz

Publications and source records attributed to Martin Scholz.

26 records · Page 2Linked to original sources

PubMed2003

[A method of computerized evaluation of CT based treatment plants in external radiotherapy].

Selection of an optimal treatment plan requires the comparison of dose distributions and dose-volume histograms (DVH) of all plan variants calculated for the patient. Each treatment plan consists generally of 30 to 40 CT slices, making the comparison difficult and time consuming. The present study proposes an objective index that takes into account both physical and biological criteria for the evaluation of the dose distribution. The DHV-based evaluation index can be calculated according to the following four criteria: ICRU conformity (review of the differences between the dose in the planning target volume and the ICRU recommendations); mean dose and dose homogeneity of the planning target volume; the product of tumour complication probability (TCP) and normal tissue complication probability (NTCP); and finally a criterion that takes into account the dose load of non-segmented tissue portions within the CT slice. The application of the objective index is demonstrated for two different clinical cases (esophagus and breast carcinoma). During the evaluation period, the objective index showed a good correlation between the doctor's decision and the proposed objective index. Thus, the objective index is suitable for a computer-based evaluation of treatment plans.

Humans↗

PubMed2003

Cariporide (HOE642) limits S-100B release during cardiac surgery.

Cardiac surgery with cardiopulmonary bypass (CPB) results in transient cerebral swelling in most patients. Cognitive decline occurs in 24-57% of patients and 2-5% experience stroke. Serum levels of S-100B, a potential marker of increased blood-brain barrier permeability, increase during and early after surgery. The authors studied the effects of the novel Na /H exchange inhibitor cariporide (HOE642) on postoperative serum levels of S-100B and neuron-specific enolase (NSE) in 53 patients at high risk undergoing coronary artery bypass grafting. Patients were randomly assigned to one of four groups: I, placebo; II, 20 mg cariporide; III, 80 mg cariporide; IV, 120 mg cariporide). In addition, the leukocyte activation marker myeloperoxidase (MPO) and malondialdehyde (MDA), a marker for lipid peroxidation, were evaluated by enzyme-linked immunoassay. Postoperatively, five patients experienced transient ischemic attack or stroke. S-100B levels increased from 0.43 microg/l +/- 0.33 before operation to 2.27 microg/l +/- 0.69 1 hour after surgery in the placebo group. Preoperative S-100B levels in the HOE642 groups did not differ from the placebo group whereas, 1 hour after surgery, levels were significantly lower in groups II, III, and IV (1.63 microg/l +/- 0.2, 1.27 microg/l +/- 0.27, and 0.90 microg/l +/- 0.21, respectively). NSE, MPO, and MDA serum levels did not differ among groups. These findings may stimulate larger clinical studies to examine the effects of HOE642 on cerebral swelling and neurologic/cognitive outcome of cardiac surgery with CPB.

Aged↗

PubMed2003

Intracerebral abscess after abutment change of a bone anchored hearing aid (BAHA).

OBJECTIVE: Brain abscesses are life-threatening and sometimes difficult to detect. A brain abscess after placement, manipulation of a bone anchored hearing aid, or a periauricular implant for fixation of an ear prosthesis has never been reported in the literature. PATIENT: A 42-year-old man suffered from a right-sided temporodorsal brain abscess after change of a bone anchored hearing aid abutment. The fixture itself had been inserted 8 years before without any complications in the peri- or postoperative period. A CT-guided puncture of the abscess could be performed via the screw-hole in the temporal bone after removal of the fixture, and the patient was treated with antibiotics. RESULTS: The outcome of the procedure was good without neurologic deficits for the patient. CONCLUSION: The insertion of periauricular screw implants bears the risk of meningeal lesions as well as a small risk of purulent intracranial and intracerebral complications perioperatively or in the context of later manipulations. Minimally invasive therapy of such brain abscesses can be performed by removal of the foreign body, CT-guided puncture, and antibiotic medication.

Adult↗

PubMed2002

Relationship between intracranial pressure and critical closing pressure in patients with neurotrauma.

BACKGROUND: The driving pressure gradient for cerebral perfusion is the difference between mean arterial pressure (MAP) and critical closing pressure (CCP = zero flow pressure). Therefore, determination of the difference between MAP and CCP should provide an appropriate monitoring of the effective cerebral perfusion pressure (CPP(eff)). Based on this concept, the authors compared conventional measurements of cerebral perfusion pressure by MAP and intracranial pressure (CPP(ICP)) with CPP(eff). METHODS: Simultaneous synchronized recordings of pressure waveforms of the radial artery and blood flow velocities of the middle cerebral artery were performed in 70 head trauma patients. CCP was calculated from pressure-flow velocity plots by linear extrapolation to zero flow. RESULTS: Intracranial pressure measured by intraventricular probes and CCP ranged from 3 to 71 and 4 to 70 mmHg, respectively. Linear correlation between ICP and CCP was r = 0.91. CPP(ICP) was 77 +/- 20 mmHg and did not differ from CPP(eff); linear correlation was r = 0.92. However, limits of agreement were only +/- 16.2 mmHg. Therefore, in 51.4% of the patients, CPP(ICP) overestimated CPP(eff) by 19.8 mmHg at most. CONCLUSION: Assuming that CPP(eff) (MAP - CCP) takes into account more determinants of cerebral downstream pressure, in individual cases, the actual gold standard of CPP determination (MAP - ICP) might overestimate the CPP(eff) of therapeutic significance.

Adolescent↗

PubMedDate not supplied

Relocalization of endothelial cell beta-catenin after coculture with activated neutrophils from patients undergoing cardiac surgery with cardiopulmonary bypass.

Cardiac surgery with cardiopulmonary bypass (CPB) is associated with neutrophil activation, inflammation, and consecutive edema. The impairment of endothelial junction molecules, and thus, hyperpermeability elicited by the interaction of activated neutrophils with endothelial cells may be important in this regard. Cocultures with human endothelial cells and neutrophils from 10 cardiac surgery patients with CPB were used to evaluate the role of neutrophils in modifications of the endothelial zonula adherens molecules VE-cadherin and beta-catenin. Laser scan microscopic analyses showed that neutrophils, which were isolated after the beginning of CPB, significantly impaired intracellular redistribution of endothelial beta-catenin with regard to membrane association (p <.0002) and staining pattern (p <.0001). VE-cadherin localization was not found to be significantly modified. Western blots with total cell extracts showed that amounts of beta-catenin did not vary significantly after co-culture with activated neutrophils. Activated neutrophils during cardiac surgery with CPB may induce endothelial dysfunction by impairing beta-catenin localization and thus contribute to endothelial hyperpermeability.

Antigens, CD↗

PubMedDate not supplied

Cardiac surgery with extracorporeal circulation: neutrophil transendothelial migration is mediated by beta1 integrin (CD29) in the presence of TNF-alpha.

Cardiac surgery with extracorporeal circulation is associated with neutrophil activation, inflammation, and edema. Endothelial hyperpermeability elicited by the interaction of activated neutrophils and/or cytokines with endothelial cells may be critical in this regard. However, the immune and cellular mechanisms involved are not fully understood. Cocultures with human endothelial cells and neutrophils from cardiac surgery patients were used to evaluate the role of beta1 integrin activity and the proinflammatory cytokine tumor necrosis factor (TNF)-alpha in neutrophil transendothelial migration and in impairment of the integrity of endothelial cell-to-cell contacts. Blocking of CD29 (heavy chain of beta1 integrins) totally prevented neutrophil adhesion and transendothelial migration. Pretreatment of neutrophils with either a CD29-stimulating monoclonal antibody or the addition of TNF-alpha (0.1-10 U/ml) to the coculture failed to induce transendothelial migration. However, coculture of endothelial cells with CD29-stimulated neutrophils in the presence of 0.1-10 U/ml TNF-alpha strongly induced neutrophil transmigration. CD29/TNF-alpha-mediated transmigration was associated with intracellular redistribution of endothelial beta-catenin. We further showed that CD29/TNF-alpha-mediated effects involved PI3K and tyrosine kinase-dependent signaling via MAPK but were independent of nuclear transcription factor (NF)-kappaB activity. Inhibition of CD29/TNF-alpha might be a therapeutic option to limit endothelial dysfunction following cardiac surgery with extracorporeal circulation.

Cell Movement↗

PubMedDate not supplied

First efficacy and safety results with the antibody containing leukocyte inhibition module in cardiac surgery patients with neutrophil hyperactivity.

Systemic administration of immune modulating antibodies may play an important role in reducing neutrophil hyperactivity, for example, in patients undergoing cardiac surgery with extracorporeal circulation or in trauma patients. However, this strategy has extremely high costs and is often associated with severe adverse effects. We developed the Leukocyte-Inhibition-Module (LIM), an extracorporeal circulation (ECC) device housing a polyurethane matrix with covalently bound Fas (CD95; APO-1) stimulating antibodies to rapidly prevent neutrophil hyperactivation. A feasibility study with 14 patients undergoing cardiac surgery with the use of immunogenic ECC without (n = 5) and with (n = 9) LIM (venous line) was performed. Our data show that the usually observed ECC associated perioperative increase in neutrophils (control) was prevented by LIM (p = 0.023). Moreover, the increase of the proinflammatory markers tumor necrosis factor (TNF)-alpha and polymorphonuclear elastase was limited by LIM (p = 0.038 and p = 0.002). In both groups, no significant changes in liver enzymes or in clotting were detected after surgery, and up to 12 months follow up, no unusual complications were reported. This study shows for the first time to our knowledge the feasibility, efficacy, and safety of a new cost effective, immune management strategy in patients with aberrant immune activation by exposing the blood stream to immobilized agonistic anti-Fas antibodies.

Antibodies↗

PubMedDate not supplied

Human cytomegalovirus infection of tumor cells downregulates NCAM (CD56): a novel mechanism for virus-induced tumor invasiveness.

Pathologic data indicate that human cytomegalovirus (HCMV) infection might be associated with the pathogenesis of several human malignancies. However, no definitive evidence of a causal link between HCMV infection and cancer dissemination has been established to date. This study describes the modulation of the invasive behavior of NCAM-expressing tumor cell lines by HCMV. Neuroblastoma (NB) cells, persistently infected with the HCMV strain AD169 (UKF-NB-4AD169 and MHH-NB-11AD169), were added to endothelial cell monolayers and adhesion and penetration kinetics were measured. The 140- and 180-kDa isoforms of the adhesion receptor NCAM were evaluated by flow cytometry, Western blot, and reverse transcription-polymerase chain reaction (RT-PCR). The relevance of NCAM for tumor cell binding was proven by treating NB with NCAM antisense oligonucleotides or NCAM transfection. HCMV infection profoundly increased the number of adherent and penetrated NB, compared to controls. Surface expression of NCAM was significantly lower on UKF-NB-4AD169 and MHH-NB-11AD169, compared to mock-infected cells. Western-blot and RT-PCR demonstrated reduced protein and RNA levels of the 140- and 180-kDa isoform. An inverse correlation between NCAM expression and adhesion capacity of NB has been shown by antisense and transfection experiments. We conclude that HCMV infection leads to downregulation of NCAM receptors, which is associated with enhanced tumor cell invasiveness.

Base Sequence↗