Systemische Freisetzung von Prostanoiden nach chirurgisch induzierter Verletzung des Lungengewebes

In a prospective study, the systemic inflammatory consequences of surgery-induced lung tissue injury were evaluated using biochemical markers. The aim was to examine whether this type of injury produces a specific pattern of prostanoid plasma levels (prostacyclin, thromboxane, PGE₂, PGF_2α, and PGM). We, therefore, compared 18 patients (group 1) who underwent thoracotomy without injury to the lung with 26 patients (group 2) that had a resection of pulmonary tissue due to benign diseases. Group 2 patients clearly revealed increased plasma levels of C-reactive protein as well as of the granulocyte-specific PMN-elastase. In particular, there was a pronounced release of prostacyclin and its antagonist thromboxane A₂ following lung tissue resection. In contrast to group 1 patients, lung tissue damage resulted in immediately elevated plasma levels of PGF_2α and PGE₂. When, however, taking into account the time course of PGM, the stable cleavage product of PGF_2α, there was no hint of an altered pulmonary metabolic capacity. Presumably, this pattern of elevated prostanoid levels in group 2 is the result of the surgical damage to the lung tissue. Therefore, it can be suggested to be specific for that type of injury. Thus, the release of prostanoids following surgery-induced lung tissue damage may indicate the importance of these mediators, particularly in thoracic injuries associated with lung damage since those may lead to post-traumatic pulmonary dysfunction. These substances may also be useful in evaluating both the severity and the extent of lung tissue damage following major trauma.     

Dopamine D2 receptor imaging with SPECT: studies in different neuropsychiatric disorders.

The purpose of the present study is to visualize and quantify dopamine D2 receptors in the living human brain using an 123I-labeled ligand and the single photon emission computerized tomography (SPECT) technique. S-(-)-Iodobenzamide [S-(-)-IBZM] has been shown to be a highly selective ligand with high affinity for D2 receptors in experimental studies. Five millicuries (185 MBq) of 123I-labeled S-(-)-IBZM was administered intravenously to 12 control subjects, 22 parkinsonian patients under L-Dopa therapy, 12 parkinsonian patients without L-Dopa, 10 unmedicated patients with Huntington's disease, and 12 patients under different neuroleptics. Data collection with a rotating double-head scintillation camera started 1 h after injection and lasted for 50 min. In a semiquantitative approach, a ratio was calculated between mean counts per pixel in the striatum and a region in the lateral frontal cortex, which was 1.74 +/- 0.10 in the control group. A marked reduction of this ratio was found in patients with Huntington's disease (1.38 +/- 0.12; p = 0.0001), no significant changes in untreated parkinsonian patients (1.67 +/- 0.14), but a reduction in L-Dopa-treated cases (1.59 +/- 0.13; p = 0.0014). A curvilinear relationship was found between total daily dose of neuroleptics and the reduction of this ratio. Estimated receptor blockade under full neuroleptic treatment was 75-80%. S-(-)-IBZM binding was reduced with increasing age (p less than 0.01). Specific binding was reduced markedly when the racemic mixture of IBZM was used, and no specific binding was seen with the R-(+)-isomer, demonstrating the stereoselectivity of IBZM binding.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of circulating anticellular antibodies by indirect immunofluorescence on HEp-2 cell substrates: study of the clinical value of rare fluorescence patterns

We detected anticellular antibodies (Ab) in 867 sera from patients with inflammatory rheumatic disorders by indirect immunofluorescence technique on HEp-2 cells and searched for clinically relevance of the rare fluorescence staining pattern (n = 133). We could find associations of 1. spekled nuclear pattern and Ab to U1-nRNP and La, 2. nucleolar pattern and scleroderma, 3. peripheral nuclear membrane pattern, Ab to dsDNA and SLE, 4. centromere staining and CRST syndrome, 5. intermedi?r filament pattern and permanent cellular destructions in erosive arthritis, 6. mitochondrial staining and inflammatory hepatic disorders. The anticellular Ab staining patterns on HEp-2 cells might be precious additionally markers for diagnosis and prognosis of inflammatory rheumatic diseases.     

Naturlatexallergie

As a consequence of AIDS prevention strategies, the use of powdered disposable latex gloves in hospitals and private medical practices has increased conspicuously in the past 10 years, and allergic reactions to natural latex have become a frequently observed problem. The clinical picture of type I allergies (immediate hypersensitivity) to natural latex ranges from slight, local allergic symptoms (urticaria, rhinitis, and conjunctivitis) to asthmatic complaints up to severest anaphylactic reactions. In addition to health care employees, patients are being affected with an increasing tendency during a variety of surgical and other medical interventions. Due to its enormous hygienic and economic significance, natural latex has become one of the most frequently studied sources of allergies. Efforts were undertaken to identify the causes and triggering factors, to develop diagnostic tools and continue to improve upon them, and to establish preventive measures and implement them successfully.     

Hereditary deficiency of antithrombin III, protein C and protein S: prevalence in patients with a history of venous thrombosis and criteria for rational patient screening.

Data in the literature on the prevalence of hereditary deficiency of the natural coagulation inhibitors are conflicting. We conducted a prospective study on 680 consecutive patients with a history of venous thrombosis to determine the prevalence of hereditary deficiency of antithrombin III (AT III), protein C(PC) and protein S(PS) and to establish selection criteria for rational patient screening. The mean age of the patients at investigation was 44.3 +/- 15.4 years, while that at the first thrombotic event was 38.5 +/- 14.8 years. The total prevalence of inhibitor deficiency states was 48/680 (7.1%). 19/680 patients (2.8%) had AT III-deficiency, 17 (2.5%) PC-deficiency, nine (1.3%) PS-deficiency and three (0.4%) a combined deficiency. In 37/48 deficient patients family studies were performed and the hereditary nature was established in 19 cases (2.8% of total patient population, six with AT III-deficiency, eight with PC-deficiency, four with PS-deficiency and one with a combined deficiency). Family studies in these 19 patients revealed 46 additional individual patients with a hereditary deficiency state. A positive family history was found in 15/19 (79%) with a proven hereditary deficiency state, in 153/619 (25%) of non-deficient patients and in 11/29 (38%) of deficient patients without established hereditary nature. The mean age at the first thrombotic event was significantly lower in patients with a hereditary deficiency state (26.8 years) compared with the other two groups (39.0 and 39.7 years, respectively). In all patients with a hereditary deficiency the first thrombotic event occurred before the age of 45 years.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dorsal root ganglia cocultured with macrophages: an in vitro model to study experimental demyelination

The present investigation introduces an in vitro model to study macrophage properties during demyelination. Rat dorsal root ganglia (DRG) were cultured for obtaining myelinated peripheral nerve fibers. These cultures were exposed to non-resident macrophages. In untreated control cultures, there was no indication of myelin removal by the added macrophages. DRG were exposed to enzymatically generated oxygen radicals using the xanthin/xanthin oxidase or the glucose/glucose oxidase system. Assessment of Schwann cell viability and ultrastructural morphology revealed different patterns of cell cytotoxicity and morphological changes in different experiments. High concentrations caused complete tissue necrosis of the DRG, while low concentrations did not affect either cell viability or ultrastructural morphology. Under intermediate experimental conditions, oxygen radicals caused non-lethal Schwann cell damage leading to Schwann cell retraction and myelin sheath rejection. Myelin lamellae were disrupted and decompacted. These changes were followed by a selective macrophage attack on myelin sheats, resulting in demyelination. Axons, Schwann cells and sensory ganglion cells survived this attack. The specificity of the oxygen radical effects was tested in experiments using the oxygen radical scavengers catalase and superoxide dismutase. Catalase prevented the described effects on cell morphology and subsequently blocked demyelination by non-resident macrophages.Supported by a grant from the Deutsche Forschungsgemeinschaft (DFG) (Br 1274/1-1)