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Biomedical subjects

N Roos

Publications and source records attributed to N Roos.

At least 73 records · Page 4Linked to original sources
PubMed1994

Artificial bone erosions: detection with magnification radiography versus conventional high-resolution radiography.

PURPOSE: To compare the diagnostic performance of direct magnification radiography with computed radiography versus that of conventional radiography in detection of artificial bone erosions. MATERIALS AND METHODS: Thirty-one paws from German shepherd dogs were embedded in paraffin and examined with x6 magnification radiography and conventional radiography before and after creation of artificial bone erosions. A microfocal x-ray unit with a focal spot of 20-130 microns was used for magnification radiography. All 210 images were analyzed by five radiologists, and receiver operating characteristic (ROC) analysis was performed. Interobserver analysis in evaluation of anatomic structures was also performed. RESULTS: ROC analysis of pooled data from all readers showed a larger area under the ROC curve for magnification radiography (0.88) than for conventional radiography (0.72). Magnification radiography produced higher scores in interobserver analysis as well. CONCLUSION: Magnification radiography is superior to conventional radiography in detection of small bone erosions.

Animals↗
PubMed1994

Tissue factor-induced coagulation triggers platelet thrombus formation as efficiently as fibrillar collagen at arterial blood flow conditions.

The relative importance of vessel wall tissue factor (TF) in initiating thrombogenesis is not well defined. In contrast, vessel wall collagens have been well documented as potent inducers of thrombus formation. We compared the potency of a human TF/phospholipid surface with that of a surface consisting of human type III collagen fibrils in triggering thrombus formation in native human blood at venous and arterial blood flow conditions. A commercial preparation, Thromborel S, was used as a source of human TF. Biochemical characterization of this preparation revealed small amounts of FVII, FIX, and FX proteins. Coagulant activity of these proteins was associated with the FVII protein only, although it was a very low activity. Studies with anti-TF antibodies in a one-stage clotting assay showed that the procoagulant activity of Thromborel was mainly a result of TF. The molar ratio of TF to phospholipid was 1:2 x 10(7). Thrombus formation in flowing nonanticoagulated human blood drawn directly from an antecubital vein was triggered by either Thromborel S or collagen fibrils coated on Thermanox coverslips in a parallel-plate perfusion chamber device. A 1:50 Thromborel S dilution gave maximal fibrin deposition (90% surface coverage) at a wall shear rate of 100 s-1. However, pretreatment of the TF surface with a monoclonal anti-TF antibody reduced this fibrin deposition by 93% (P < .001). Thus, TF was essential for the procoagulant activity of the Thromborel S surface in this flow system also. At higher wall shear rates (650 and 2600s-1), less fibrin was deposited, but the platelet thrombus formation on the fibrin mesh increased dramatically.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗
PubMed1993

Transfer of retinol-binding protein from HepG2 human hepatoma cells to cocultured rat stellate cells.

Rat liver stellate cells were cocultured with HepG2 human hepatoma cells, which are known to synthesize and secrete retinol-binding protein (RBP). Transfer of human RBP from HepG2 cells to stellate cells was studied by cryoimmunoelectron microscopy. In stellate cells, human RBP was found on the cell surface and within endosomes. The transfer of human RBP from HepG2 cells to stellate cells was blocked by addition of RBP antibodies to the culture medium. Very little uptake of RBP was observed when fibroblasts were cocultured with HepG2 cells. In a series of experiments, RBP was bound to its putative cell surface receptor at 4 degrees C, and the stellate cells were washed and then incubated at 37 degrees C in order to allow them to internalize a pulse of RBP. About 50% of the RBP was internalized after 6 min of incubation. The RBP-positive vesicles were initially (after 1-2 min) located close to the cell surface and later were found deeper in the cytoplasm. During the first 10 min, RBP was mainly observed in close association with membranes. After 2 hr, however, most RBP was localized in intracellular vesicles at a distance from the vesicular membranes, suggesting that RBP had been released from its receptor. Saturable binding of RBP to liver cells was demonstrated when cells were incubated with 125I-RBP at 4 degrees C and cell-associated radioactivity was determined. The calculated dissociation constant for the specific binding was 12.7 +/- 3.2 nM. A binding assay was also developed for determination of solubilized RBP receptor. Solubilized proteins from the nonparenchymal liver cells bound about 30 times more 125I-labeled RBP than did parenchymal cells (based on mass of cell protein). These data suggest that RBP mediates the paracrine transfer of retinol from hepatocytes to perisinusoidal stellate cells in liver and that stellate cells bind and internalize RBP by receptor-mediated endocytosis.

Animals↗
PubMed1993

Mechanical ventilation in the prone position for acute respiratory failure after cardiac surgery.

Ten patients with acute respiratory failure (ARF) after coronary artery bypass grafting were studied during conventional mechanical ventilation in the supine and in the prone position. Impaired gas exchange was defined as an inspired oxygen fraction (FIO2) greater than 0.5 to maintain an arterial oxygen tension (PaO2) > or = 70 mmHg, an alveolar-arterial PaO2 gradient (PA-aO2) > 200 mmHg and a venous admixture (QVA/QT) > 15% during mechanical ventilation with a tidal volume (VT) = 10 to 12 mL/kg, frequency (f) = 10 to 15 VT/min, inspiratory-expiratory (I:E) ratio = 0.5, and positive end-expiratory pressure (PEEP) of 5 to 7.5 cm H2O. In the supine position, systemic and pulmonary hemodynamics were in the normal range, but oxygenation was severely impaired. In all patients thoracic computed tomography scans were obtained and revealed crest-shaped bilateral densities in the dependent lung regions. FIO2 of 0.67 +/- 0.22 was required to maintain a PaO2 greater than 70 mmHg during mechanical ventilation in the supine position. Under these conditions PA-aO2 and QVA/QT were 362 +/- 153 mmHg and 32.5 +/- 8.3%, respectively. CO2 elimination was not severely affected. The patients were turned into the prone position after an average of 30.6 +/- 5.4 hours postoperatively and ventilated with unchanged VT, f, PEEP, and inspiratory-expiratory ratio for 26.7 +/- 11.7 hours (range, 10 to 42 hours). A second cardiopulmonary status was obtained within 2 to 5 hours of ventilation in the prone position.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

In-vitro high-resolution ultrasonography of benign and malignant lymph nodes. A sonographic-pathologic correlation.

RATIONALE AND OBJECTIVES: The authors assess the value of combining high-resolution ultrasonography (HRUS) findings in a scoring scale for distinguishing malignant from reactive lymphadenopathy and explain the pathologic causes of altered nodal sonographic architecture. MATERIALS AND METHODS: Sixty-one nodes obtained from 32 consecutive patients were prospectively scanned with 7.5-MHz ultrasound probes in a waterbath. Three sonographic features--long-to-short axis ratio (L/S), hilar width, and cortical width--were graded on a 5-level scoring scale (0-4). Nodes scored > or = 3 were considered malignant and < or = 2 benign. Subsequently, all nodes were microsectioned in a plane matching the sonograms, allowing direct sonographic-pathologic correlation. RESULTS: Eighty-two percent of nodes were correctly characterized using the above cut-off point (sensitivity: 87%, specificity: 74%). Eighty-three percent of nodes scored 4 were malignant and 95% scored 0 were benign. Eighty-two percent of nodes with L/S < 2, 81% with no hilus, and 70% with eccentric cortical widening were malignant, whereas 72% with L/S > or = 2, 86% with a wide hilus, and 91% with a narrow cortex were benign. Sonographic-pathologic correlation showed that tumor infiltration results in rounded nodal shape, loss of hilar echogenicity and cortical widening, whereas reactive disease tends to preserve nodal architecture. CONCLUSION: Morphologic changes detectable using HRUS help distinguish benign from malignant lymph nodes.

Diagnosis, Differential↗
PubMed1993

Hepatic uptake of beta-VLDL in cholesterol-fed rabbits.

The hepatic uptake of intravenously injected beta-very low density lipoprotein (beta-VLDL) in rabbits fed 2% (w/w) cholesterol for 3 weeks was investigated. In vitro studies were also conducted to examine the specificity and the capacity of the uptake in isolated liver parenchymal cells. The hepatic uptake of beta-VLDL was 15.8 +/- 6.7% (n = 6) in the cholesterol-fed rabbits as compared to 26.6 +/- 7.5% (n = 6) of the injected dose in control rabbits (P < 0.05). Although this is a fractional reduction, it represents a more than 10-fold increase in absolute hepatic uptake of lipoproteins in the cholesterol-fed rabbits. In these animals the liver parenchymal, endothelial, and Kupffer cells took up 10.2 +/- 2.7%, 3.0 +/- 0.9%, and 1.8 +/- 0.4% of the injected dose, respectively, compared to 25.9 +/- 6.1%, 3.6 +/- 1.6%, and 1.5 +/- 0.8% of the injected dose in chow-fed controls. However, taking into account the high plasma lipoprotein levels in the cholesterol-fed rabbits, the absolute cellular uptake was 10-fold increased in the parenchymal liver cells and more than 20-fold increased in the nonparenchymal cells. In vitro results indicated a 40% down-regulation of the specific receptor for beta-VLDL in the parenchymal cells, and this, together with an increased competition for binding sites in the hypercholesterolemic rabbits, probably explains the reduced uptake of beta-VLDL in terms of % of injected dose observed in vivo. In vitro data suggested that the receptor involved in both hypercholesterolemic and normolipemic rabbits was the apolipoprotein (apo) B,E receptor. On a per cell basis, parenchymal cells from chow-fed control animals took up 2.4 +/- 0.8% of the injected dose per 10(9) cells; this uptake was reduced to 1.1 +/- 0.5% in hypercholesterolemic animals. No differences in uptake of beta-VLDL in nonparenchymal liver cells were observed on a per cell basis between the two feeding groups, indicating that binding sites involved in this uptake are not down-regulated by cholesterol feeding. On the contrary, the absolute uptake in the nonparenchymal liver cells is greatly increased in hypercholesterolemic rabbits as compared to controls. In cholesterol-fed rabbits the three different liver cell types took up approximately the same amount of beta-VLDL per cell. The liver nonparenchymal cells, therefore, assume a prominent role in uptake of beta-VLDL in hypercholesterolemic rabbits, accounting for more than 30% of the total hepatic uptake as compared to 16% in control animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Receptor-mediated endocytosis of ricin in rat liver endothelial cells. An immunocytochemical study.

The endocytic pathway of ricin in sinusoidal liver endothelial cells (EC) was traced by means of immunocytochemical labeling of ultrathin cryosections. Ricin, a highly mannosylated glycoprotein, is internalized mainly by receptor-mediated endocytosis via the mannose receptor in the EC. Labeling of specimens fixed at different time points after injection of ligand showed that several subcellular compartments are involved in processing of endocytosed ricin. One minute after injection ricin is seen in coated pits, coated vesicles and cisternal-shaped endosomes. After 6 min, the ligand associates with electron-dense, spherical vesicles and electron-lucent vesicles, presumably representing late endosomes. In the same time period we observed labeling in the vicinity of the Golgi stack. At later time points, ricin is increasingly localized in lysosomes. Both late endosomes and lysosomes showed labeling for Igp120, the lysosomal membrane glycoprotein. To compare uptake of ricin with another mannosylated ligand, we coinjected ricin and mannosylated colloidal gold particles (Man-Aun). Man-Au20, injected 24 h before fixation as a marker for late endocytic compartments, was found in two distinct compartments, presumably representing late endosomes and lysosomes. The distribution of ricin and Man-Au10, the latter injected 15 min before fixation, in early endosomes was strikingly different, indicating that the structure of this compartment is important in the process of sorting of ligand and receptor.

Animals↗
PubMed1993

[Postmortem high-resolution computed tomography of the lung. Radiologic-morphologic correlations].

To establish precise correlations between high-resolution computed tomography (CT) and normal pulmonary anatomy and pulmonary pathology, 49 lungs affected by different diseases were analysed. Post-mortem high-resolution CT scans were compared with the corresponding macroscopic and microscopic pathological findings. For scanning, lungs were inflated and fixed, which avoided any decrease in the structural resolution of pulmonary parenchyma and allowed a topographically exact correlation between CT appearances and morphological changes. After demonstration of the structural details relevant for CT in normal pulmonary parenchyma, an attempt is made to establish the morphological basis of the following CT phenomena: thickening of interlobular septae, increase in pulmonary translucency, consolidation of the non-nodular alveolar and of the nodular type, and changes in the pleural region. Although CT findings in pulmonary lesions are mainly non-specific, knowledge of the corresponding morphological basis is helpful in diagnostic evaluation.

Animals↗
PubMed1993

[Computed tomography in noninfectious interstitial lung diseases].

Computed tomography is a well-established imaging technique for the assessment of non-infectious interstitial pulmonary disease. Compared with the conventional chest radiograph it is characterized by a higher degree of sensitivity and specificity, particularly when a high-resolution technique is implemented. Because of its superior correlation with the morphological characteristics in specific diseases, it plays an important role if the histological diagnosis is doubtful and also in patients with clinical features suggestive of pulmonary disease in the presence of a normal chest film. This article describes the limitations of the conventional chest radiograph and the advantages of pulmonary computed tomography. Typical CT findings in different interstitial diseases are illustrated, and their value is discussed in comparison with the plain radiograph.

Asbestosis↗
PubMed1992

Evidence for carbohydrate-independent endocytosis of tissue-type plasminogen activator by liver cells.

In the liver, tissue-type plasminogen activator (t-PA) is endocytosed by hepatic parenchymal (PC), endothelial (EC) and Kupffer (KC) cells. Although the endocytosis is receptor-mediated, it remains a matter of discussion which receptors are involved in this catabolic process. To evaluate the role of a protein-specific receptor, as well as the possible involvement of the galactose receptor on PC and the mannose receptor on EC, we have employed different glycosylation variants of t-PA in biochemical and immunocytochemical studies. Partial or total removal of carbohydrate side-chains by endoglycosidases did not prevent clearance and hepatic endocytosis of t-PA by either of the liver cell types. Blockade of the galactose and mannose receptors by co-application of a large excess of the glycoprotein ovalbumin remained without effect on the binding and uptake of t-PA by hepatic cells. However, the contribution of different liver cell types to the hepatic clearance of t-PA was to a certain extent dependent on the type of oligosaccharide chains removed. The mannose receptor on EC is partially responsible for the clearance of t-PA by this cell type, whereas the galactose receptor does not seem to be involved in this process. The results obtained in this study further demonstrate that the major portion of the hepatic catabolism of t-PA is independent of its carbohydrate side-chains.

Amidohydrolases↗
PubMed1992

Endocytosis and intracellular processing of tissue-type plasminogen activator by rat liver cells in vivo.

Endocytosis of tissue-type plasminogen activator (t-PA) by different types of rat liver cells was studied in immunocytochemically labelled cryosections as well as in biochemical experiments. For morphological localization of the ligand in different endocytic compartments involved in its catabolism, rat livers were fixed at various times (1-24 min) after injection of t-PA. Late-endosomal and lysosomal compartments were identified by double-labelling the sections with antibodies to the lysosomal proteins glycoprotein Igp 120 and cathepsin D. In liver t-PA was localized in sinusoidal endothelial cells (EC), parenchymal cells (PC) and to some extent in Kupffer cells (KC), indicating that it is internalized and degraded in all three cell types. In specimens fixed 6 min after injection PC, EC and KC were found to contribute to 69, 24 and 7% respectively of total t-PA endocytosed. The transfer from late endosomes to lysosomes was found to be faster in EC than in PC. The morphological findings were supported by studies of the endocytic mechanisms employing isolated perfused livers and primary hepatocytes. The presence of monensin, an inhibitor of lysosomal protein degradation, reduced the amount of t-PA degraded to about 50% of the control values. The catalytic site seems not to be required for the catabolism of t-PA in hepatic cells. The inhibition of t-PA by D-phenylalanyl-L-prolylarginyl-chloromethane did not influence receptor recognition and catabolic processing, as determined in morphological studies using labelled cryosections, in binding studies employing liver cell membranes and primary hepatocytes, as well as in liver-perfusion experiments.

Animals↗
PubMed1992

Antifungal treatment strategy in leukemia patients.

Among the opportunistic infections in patients with leukemias systemic fungal infections contribute a major part if not the majority. This results from autopsy data and is supported clinically when using new criteria by imaging techniques, while microbiological documentation shows a low sensitivity in this situation. Those lessons require a change in strategy toward an earlier and empiric use of systemic antifungal drugs in the frequent infections appearing as fever of unknown origin. By its high systemic activity and low toxicity Fluconazole facilitates this approach. Amphotericin B with 5-Flucytosine remain as the most established standard. Liposomal Amphotericin B allowing higher dosage by lower toxicity appears effective as salvage treatment especially in aspergillosis which also responds to Itraconazole available as oral formulation so far.

Amphotericin B↗
PubMed1992

Invasive aspergillosis complicating induction chemotherapy of childhood leukaemia.

Two children with acute leukaemia developed histologically confirmed invasive aspergillosis within 2 weeks after onset of polychemotherapy. One child had received only prednisone and one pulse of vincristine and daunorubicin before. This child showed classical roentgenographic signs of aspergilloma following an upper pulmonary lobe infiltration. The second patient developed caecal aspergillosis obscured by clinical signs of appendicitis. He died of disseminated aspergillosis several weeks later in spite of systemic antifungal therapy. Both case reports illustrate that the possibility of invasive aspergillosis must also be expected in young patients soon after onset of induction chemotherapy.

Aspergillosis↗
PubMed1992

Therapeutic use of surfactant in neonatal respiratory distress syndrome. Correlation between pulmonary X-ray changes and clinical data.

As part of a multicenter surfactant rescue study, the chest X-rays of 239 preterm and term infants were analyzed. To study the influence of surfactant administration on radiographic appearance, 130 patients with a clinical and radiological diagnosis of typical respiratory distress syndrome were selected, in whom adequate chest x-rays before and within 48 h after treatment were available. Median gestational age was 30 weeks (range 25-38 weeks), median birth weight was 1335 g (range 625-3450). The time of surfactant application ranged between 90 min and 24 h after birth (median 6 h). The most common finding after surfactant administration was uniform (n = 47) or disproportionate (n = 46) improvement of pulmonary aeration, which showed a significant correlation to posttreatment reduction of oxygen requirement (p less than 0.0001). Asymmetric clearance was more often localized on the right side and usually disappeared within two to five days. Only in 13 patients no change of ventilation was found. Development of interstitial emphysema (n = 24, including three patients with pneumothorax) after surfactant treatment was an unfavourable prognostic sign. 54% of these patients (13 of 24) died within the first month of life, compared to 8% (7 of 93) in the group of patients with initial improvement of ventilation.

Female↗
PubMed1992

Immunomorphologic and biochemical identification of the pemphigus foliaceous autoantigen within desmosomes.

Desmosomes are specialized domains of the plasma membrane that play a fundamental role in intercellular adhesion. This adhesive function is mediated at least in part by the cadherin homologous cell adhesion molecule (CAM) desmoglein (dg). Autoantibodies (aab) from patients with pemphigus foliaceous (pf), a blistering disease of the epidermis, have been shown by immunochemical methods to bind to desmoglein. However, the molecular localization of the binding sites of these antibodies, especially as it relates to the ultrastructure of the desmosomes, has not been definitively characterized. We therefore performed pre-embedding direct immunoelectron microscopy (IEM) on perilesional skin of patients with pf and post-embedding indirect IEM using sera from five patients with pf. We first confirmed by immunoprecipitation and immunoblotting that these sera bound dg. Both IEM methods showed that pf-aab exclusively bind to desmosomes. Double-labeling IEM of several other constitutive desmosomal proteins further suggests that most likely pf-aab bind to an extracellular domain of the transmembrane CAM dg. Our studies suggest one possible pathophysiologic mechanism for the clinical manifestations of pf: namely, that the binding of aab to an extracellular epitope of desmoglein might impair the adhesive properties of desmosomes mediated by dg and result in the loss of cell adhesion leading to acantholysis and blister formation.

Autoantigens↗
PubMed1992

Gas exchange impairment and pulmonary densities after cardiac surgery.

In 11 patients with impaired respiratory function after coronary artery revascularization surgery, thoracic computed tomography (TCT) and cardiopulmonary profile were obtained. The patients were haemodynamically stable without clinical or radiological signs of lung oedema. Oxygenation was reduced in all patients (alveolo-arterial PO2-difference (PA-aO2) = 37.3 +/- 10.39 kPa, venous admixture (QVA/QT) = 26.4 +/- 4.4%) during mechanical ventilation with positive end-expiratory pressure (PEEP = 5 cmH2O) (0.5 kPa). TCT-scan analysis revealed considerable amounts of crest-shaped bilateral densities in dependent lung regions. There were no differences between the right and left hemithorax. Atelectatic lung tissues were defined as areas presenting with attenuation values of -200 to +20 Hounsfield Units. The magnitude of non-ventilated areas correlated with QVA/QT (r = 0.875, P < or = 0.01), but not with the duration of either extracorporeal circulation, surgical procedure or general anaesthesia. It is concluded that atelectasis in dependent lung areas contributes to impaired gas exchange after cardiac surgery.

Aged↗