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The microanatomical structure of human and rat splenic white pulp is compared, with special emphasis on the localization of the marginal zone occupied by immunoglobulin M (IgM)+ IgD-/dull B lymphocytes and its specialized macrophages. Our study reveals that in contrast to rats, the marginal zone of humans primarily exists in the vicinity of primary and secondary splenic follicles and that it is almost absent around the periarteriolar T-cell zones. We demonstrate that in humans there is an additional compartment, the perifollicular zone, located between the marginal zone and the red pulp. The perifollicular zone is a dynamic region of variable cellular and phenotypic composition, which can be regarded either as a part of the red pulp or of the follicles. In most cases the perifollicular zone appears as a compartment of the red pulp containing erythrocyte-filled spaces which differ from the typical red pulp sinusoids. Similar to the splenic cords, the perifollicular zone mostly harbours scattered B and T lymphocytes. However, sometimes B lymphocytes clearly predominate in the perifollicular area. In addition, strongly sialoadhesin-positive macrophages form sheaths around capillaries in the perifollicular zone. Such capillary sheaths are not observed in rats. In humans weakly sialoadhesin-positive macrophages are also present in the perifollicular zone and in the red pulp. In some specimens sialoadhesin is, however, strongly expressed by a large number of dispersed perifollicular macrophages. Interestingly, in striking contrast to rats, the human marginal zone does not contain sialoadhesin-positive macrophages and marginal metallophilic macrophages are also absent in humans. Thus, sialoadhesin-positive macrophages and IgM+ IgD- memory B lymphocytes both share the marginal zone as a common compartment in rats, while they occupy different compartments in humans. We show that the human splenic marginal zone does not contain a marginal sinus and assume that in humans the perifollicular region is the compartment where antigen and recirculating lymphocytes enter the organ.

Wenn uber einen Zeitraum von 6 Monaten hinaus, an mehreren Tagen gemessen, Calcium- und Parathormonkonzentrationen im Serum unterhalb des Normbereiches liegen, sprechen wir von permanentem Hypoparathyreoidismus. Er ist symptomatisch, wenn Beschwerden und/oder Folgeerkrankungen auftreten, die mit diesem Mangelsyndrom verbunden sind bzw. mit ihm assoziiert werden.

This study was performed to analyse the correlation between vascular surface (VS), tumour grade and stage and relative proportion of tumour cells within the tumour stroma. Specimens of 41 prostatic carcinoma were immunostained using Factor VIII-related antigen. The VS was assessed by means of stereology. In tumour-free prostatic tissue the VS was 6.7 ± 0.4 mm−1. In pT2 tumours this value was significantly increased to about 12 mm−1. With rising pT stage the VS significantly decreased to values of 4 in pT4 tumours. In G1 tumours the VS was 14.6 mm−1 and significantly decreased with decreasing grade of differentiation. No significant difference was obtained between pN0 and pN + cases. A close positive correlation (r = 0.59,P < 0.001) existed between the VS and the relative proportion of tumour cells within the tumour, whereas a strong negative correlation was found between the VS and the relative amount of tumour stroma (r = 0.81,P < 0.001). The VS mainly depends on tumour differentiation and pT stage, i.e. the tumour size and the relative proportion of stroma and tumour cells within the tumour. These results are consistent with those obtained in experimental tumours. Assessment of the VS is therefore of interest in studies of tumour biology; it is of no use in predicting lymph node metastasis.

Aufgrund der vielfaltigen Stoffwechselfunktionen des Parathormons ist die medikamentose Therapie des permanenten Hypoparathyreoidismus von allen endokrinen Unterfunktionstorungen am schwierigsten. Ziel ist deshalb die kausale Therapie dieses Mangelsyndroms, die Allo- oder Xenotransplantation der Parathyreoidea. Der Bedarf, allein fur die BR Deutschland, wird auf mindestens 1500 Transplantationen pro Jahr geschatzt.

Microencapsulation of tissues is an alternative to postoperative immunosuppression in transplantation. In 1994 iso-, allo- and xenotransplantation of microencapsulated parathyroid tissue was achieved in vivo. However, continued analysis of the coating substance (an alginate) determined mitogenic properties. Here, we report on the in vitro and in vivo function of parathyroid tissue microencapsulated with a novel amitogenic alginate suitable for use in humans. To assess in vitro function, parathyroid tissue encapsulated with mitogenic and amitogenic alginate was exposed to rising concentrations of calcium. For in vivo experiments, it was isotransplanted into parathyroidectomized rats. PTH release into medium and PTH serum levels as well as calcium levels of recipient rats were analyzed and compared to native (non-microencapsulated) tissue and empty capsules, respectively. In vivo, transplants were excised and subjected to histologic examination six months after trans-plantation. In vitro, parathyroid tissue encapsulated with amitogenic alginate releases approximately half of the PTH of native tissue, not different from tissue encapsulated with the mitogenic alginate. In vivo, the novel alginate preserved parathyroid function similar to that of native tissue over the six month period resulting in complete reversal of hypoparathyroidism. Correspondingly, histologic examination revealed vital parathyroid tissue in intact microcapsules. By establishing in vitro function and successful long-term transplantation, we have documented the principle of microencapsulation of parathyroid tissue to be effective also with the novel amitogenic alginate, which is suitable for clinical use.

Prostatic carcinoma obtained from 41 patients (pT2N0, 5; pT2N+, 2; pT3N0, 16; pT3N+, 16; pT4N0, 1; and pT4N+, 1) ranging from 45 to 79 years of age were investigated in the present study. A total of 410 tumor areas of different grades were analyzed (G1, n = 116; G2, n = 98; and G3, n = 196). Vascular structures were labeled immunohistochemically using factor-VIII-associated antigen. The vascular surface density (VSD), the microvessel number (NVES), and the maximum microvessel number (NVES-MAX) were assessed by means of stereology, and the results were related to tumor stage, nodal status, and grade of differentiation. NVES and NVES-MAX showed a significant increase with rising pT stage ranging from 25.5 +/- 1.48 in controls to 135.0 +/- 5.5 microvessels/mm2 in pT4 tumors. Discrimination of different pT stages was more accurate with NVES-MAX. The VSD was significantly higher in pT2 tumors compared with controls, whereas there were no significant differences between pT3 tumors, pT4 tumors, and controls, although the values in pT3 and pT4 tumors were distinctly lower than in pT2 tumors (P.05). The VSD and the NVES were not able to discriminate between the pN0 and the pN+ group. Both parameters were slightly higher in patients with metastatic disease. Only NVES-MAX values differed between the two groups with an average of additional 21 microvessels/mm2 in the pN+ group (P.05). Concerning the grade of tumor differentiation the VSD continuously decreased from G1 (14.58 +/- 2.24 mm(-1) to G3 tumor areas (5.41 +/- 1.46 mm(-1). Only G1 tumors showed significant differences compared with controls (6.65 +/- 0.38 mm(-1). The NVES increased with rising tumor grade with significant differences between all four groups ranging from 25.5 +/- 1.5 in controls to 136.9 +/- 37.2 microvessels/mm2 in pT4 tumors.

Objective To evaluate the extent of vascularization by assessing vascular surface density in renal cell carcinomas (RCCs) of different nuclear grades, and in normal renal cortex and medulla. Materials and methods Specimens of 79 RCCs of different nuclear grades (16 of G1, 42 of G2 and 21 of G3) were immunostained with the lectin Ulex europaeus agglutinin-I (UEA I). The vascular surface density of tumour tissue was assessed stereologically using a test grid at ×400 magnification and compared to the values obtained in normal renal tissue. Results G3 tumours had a lower vascular surface density than had G1 and G2 RCCs and normal renal tissue of the cortex and medulla (P

The active metabolite of vitamin D 1,25-dihydroxycholecalciferol is a hormone-like agent that regulates cell differentiation and proliferation. Various vitamin D derivatives have been shown to induce differentiation in neoplastic cells. The prerequisite for any hormone action is the presence of its receptor. We studied the expression of vitamin D receptor in human lung cancer cell lines and in primary lung cancer tissue. Employing the polymerase chain reaction, 10 out of 11 cell lines stemming from small-cell lung cancer and 15 out of 15 cell lines stemming from non-small-cell lung cancer demonstrated vitamin D receptor expression. An immunohistochemical analysis, using a specific monoclonal antibody, demonstrated vitamin D receptor protein expression in 31 out of 117 (26%) primary small-cell lung cancer cases tested. Positive cells exhibited a nuclear reaction pattern. Twenty-one out of 37 primary non-small-cell lung cancer cases, particularly adenocarcinomas (9/14) and squamous-cell carcinomas (10/15), exhibited vitamin D receptor. Results indicate that a subset of lung cancer cases may be susceptible to the differentiating effects of vitamin D analogues.

The traditional approach of solving a linear pseudo-Boolean optimization problem (maximize a linear pseudo-Boolean term cL subject to a set of linear pseudo-Boolean inequalities S) is to solve the linear programming relaxation of the problem and then to branch on a variable Xi having a fractional value in the current LP-solution. If there is no such variable, then the LP-optimum is the integer optimum. Branching on Xi yields the two subproblems maximize cL subject to S, Xi = 1 and maximize cL subject to S, Xi = 0, which are solved recursively by the same approach. The desired optimum is the maximum of the optima of the two subproblems. Subproblems need not be split further if either all variables are integral or if there is another subproblem having an integral solution with a greater value of the objective function.

Transforming linear pseudo-Boolean inequalities into an equivalent set of extended clauses allows us to handle linear pseudo-Boolean constraints with specialized methods for extended clauses [Bar93c, Bar94]. Furthermore, deciding whether a linear pseudo-Boolean inequality is dominated by a set of pseudo-Boolean constraints reduces to the simpler problem of deciding whether extended clauses are dominated; an issue for which our solved form of pseudo-Boolean constraints is well-suited.

The declarative paradigms constraint solving and logic programming are successfully merged in constraint logic programming. Integrating constraint solving techniques into logic programming increases expressibility, efficiency, and flexibility and therefore encourages declarative programming. Efficient special purpose algorithms, coming from mathematics, operations research, or artificial intelligence, can be embedded into the logic programming language. The logic programming language allows one to declaratively state the problem, which is solved by the underlying constraint solver. Besides being a high-level declarative interface to the constraint solver, the logic programming language allows the implementation of subproblems that do not fit into the constraint domain.

After a formal presentation of the constraint domain PB we investigate several methods for solving pseudo-Boolean constraints and examine their applicability in the context of constraint logic programming. We adopt a logical view of pseudo-Boolean constraints and propose a solved form suitable for the constraint logic programming language CLP(PB).

We outline a constraint solver for pseudo-Boolean constraints based on the generation of logic cuts. The principle idea is to add logic cuts to the current set of constraints as long as an appropriate relaxation of the problem is not able to answer the questions imposed by the current state of the CLP-program.

To evaluate four automated devices to achieve transthoracic lung biopsy. Transthoracic lung biopsy specimens were obtained randomly from 21 human cadavers with unsuspicious lungs using Biopty (18- and 20-gauge), BIP (18 and 20-gauge), ASAP (18 gauge), and Autovac (18- and 20-gauge) devices. A total of 63 biopsies were carried out with each device and each needle diameter. The same devices and needles were then used randomly for biopsy of peripheral lung metastases. Specimens obtained during both parts of the study were analyzed for the area of tissue on the histologic section, adequacy of tissue for diagnosis, tissue preservation, and crush artifact. The examining pathologist was kept unaware of which procedure was used to obtain the specimens and the cadavers' clinical history. The Biopty 18-gauge device performed statistically better than any other of the evaluated systems for biopsy of normal lung parenchyma (p < 0.05). For biopsy of lung metastases, the differences between the devices and needle diameters were less, although the Biopty 18-gauge device performed better than the Autovac 18-gauge, BIP 18-gauge, and all 20-gauge devices for the area of tissue on the histologic section (p < 0.05). The results of the full-cut Autovac biopsy system were remarkable because of the large number of biopsies during which no tissue was obtained. Automated biopsy devices can obtain high quality lung specimens sufficient for definite histopathologic diagnosis. However, additional clinical studies on the use of automated biopsy devices for lung biopsy are mandatory.

Nitrogen dioxide (NO2), the oxidation product of nitric oxide (NO), is a reactive free radical forming gas, the inhalation of which has been reported to induce severe damage to distal airways. In order to quantify dose and time course of parenchymal and vascular damage, rats were exposed to 5, 10 and 20 ppm NO2 for 3 and 25 days, followed by quantitative histology and morphometry of the lung. Histological investigations of the short-term exposed animals showed structural alterations extending from slight interstitial oedema after exposure to 5 ppm, to epithelial necrosis and interstitial inflammatory infiltration after exposure to 10 ppm, and an additional intra-alveolar oedema after 20 ppm. The pulmonary arteries disclosed no qualitative changes, such as muscularization of intra-acinar vessels. Long-term exposure to 10 ppm and 20 ppm NO2 resulted in emphysema and slight centrilobular interstitial fibrosis. Morphometric analysis revealed the alveolar surface density to be significantly diminished after short-term exposure to 20 ppm NO2 and long-term exposure to 10 and 20 ppm NO2. The medial thickness of pulmonary arteries was significantly increased after short- and long-term exposure to 20 ppm NO2 and long-term exposure to 10 ppm NO2. In the 5 ppm short- and long-term exposure groups the pulmonary arterial medial thickness was significantly decreased compared to controls. Correlation analysis revealed a negative correlation between average medial thickness and alveolar surface density (coefficient of correlation: -0.56). We conclude that the extent of NO2-induced pulmonary parenchymal and vascular alterations are closely related and concentration- and time-dependent.

(1994). Primary Osteosarcoma of the Breast—Case Report and Review of the Literature. Acta Oncologica: Vol. 33, No. 1, pp. 74-76.

To study the effects of nitrogen dioxide (NO2) inhalation on lung lavage surfactant components as markers of an altered surfactant metabolism in type II pneumocytes, rats were exposed to atmospheres with increasing NO2 concentrations (0.8, 5.0, and 10.0 ppm) over 1 and 3 days. After exposure lung lavage was performed and surfactant components as well as lavageable cells analyzed. An increased number of total lavage cells was found with increasing concentration and duration of NO2 exposure. Cell distribution showed an elevation in the number of granulocytes and lymphocytes whereas the number of macrophages was diminished. The amount of total lavage protein revealed an increase related to NO2 concentration and duration. Also the content of lavage phospholipid was increased, with a decreased portion of phosphatidylcholine (PC). Further analyses of PC showed a diminished composition of saturated fatty acids but an elevated content of the unsaturated portion. Functional studies on surfactant phospholipid extracts exhibited comparable values for the surface tension at equilibrium, as well as for the maximal and minimal surface tension of animals exposed to 0.8 ppm NO2 and controls. Higher NO2 concentrations (5 and 10 ppm) resulted in increased values for surface tension compared to controls. This was also observed with purified surfactant that was obtained from controls and from NO2-exposed rats. These experiments show that in vitro exposure of purified surfactant to NO2 atmospheres was more effective than exposure in vivo. When the structure of the surfactant proteins A was studied it was found not to be altered by the NO2. The data clearly demonstrate that NO2 inhalation impaired function of surfactant components that may be used as markers of altered surfactant metabolism.

4039 Background: Chemotherapy with gemcitabine is the standard adjuvant or additional treatment in R0- or R1-resected pancreatic cancer. Adding cetuximab is suggested to improve the outcome of thes...

Inspired by the globule arc technique a new electrothermal vaporization inductively coupled plasma optical emission spectrometry (ETV-ICP OES) method was developed for the analysis of high-purity copper materials. The performance of the method was investigated for the analytes Ag, Al, As, Bi, Cd, Co, Cr, Fe, Mg, Mn, Ni, P, Pb, S, Sb, Se, Si, Sn, Te, Ti, Zn and Zr. ETV parameters were optimized regarding the release of the analytes, the transport efficiency and the quality of analytical results in terms of precision, trueness and power of detection. The influence of CCl2F2, CHClF2, C2H2F4 and CHF3 as gaseous halogenation modifiers was investigated. A sufficient in situanalyte matrix separation was achieved by using CHF3 as halogenating reagent avoiding a high matrix input from the molten copper sample into the ETV system and the plasma. A complete release from the samples was obtained for all investigated analytes except Se and Te. Acceptable results for the determination of the trace elements Ag, Al, As, Bi, Cd, Co, Cr, Fe, Mg, Mn, Ni, P, Pb, S, Sb, Si, Sn, Ti, Zn and Zr in high-purity copper were achieved. The method includes a preceding sample preparation step of oxidizing the surface of copper samples which results in a significantly enhanced sensitivity. In addition to the calibration with copper samples, the feasibility of the calibration with liquid multi-element solutions was investigated. Except for Ag, Mg and Ni all analytes could be analyzed using aqueous calibration solutions. The trueness of the method was tested by the determination of analyte contents of certified reference materials. Limits of quantification ranging from 0.6 ng g−1 to 29 ng g−1 were achieved. The developed direct solid sampling method is time and cost effective and well suited for the characterization of high-purity copper materials. The method can be automated to a large extent and is applicable for processes accompanying analyses. In contrast to all other investigated trace elements, Se and Te were not released from the matrix at measurable levels under the used conditions. The determination of these elements is still under investigation and will be reported in a succeeding publication.

Various drugs have been shown to stimulate surfactant phospholipid metabolism. Particularly beta-adrenergic agonists play an important role under physiologic conditions. For the first time we have studied whether nitrogen dioxide (NO2) inhalation alters beta-adrenergic regulation of surfactant phospholipid metabolism in the model of the isolated lung. Rats were continuously exposed in vivo to a 5 ppm NO2-containing atmosphere for 48 hr. The lungs were isolated and perfused in presence of the beta-adrenergic agonist dopexamine and surfactant metabolism was studied in three lung compartments: (1) lung lavage, (2) lung tissue, and (3) lavagable free alveolar cells. We found that (1) in normal rat lungs dopexamine increased the incorporation of palmitate and choline from the perfusate into lung lavage phospholipids. In nitrogen dioxide exposed rat lungs beta-adrenergic stimulation did not cause an increase in precursor incorporation. No significant difference in unstimulated precursor incorporation was found for normal and NO2-exposed rat lungs. (2) Lung tissue from rats exposed to NO2 showed a decreased precursor incorporation into disaturated phosphatidylcholine due to an augmented cellular pool size. (3) Lavagable alveolar cells showed an increased palmitate uptake after nitrogen dioxide inhalation and by beta-adrenergic stimulation. From these data we conclude that nitrogen dioxide inhalation impairs the beta-adrenergic regulation of surfactant phospholipid metabolism. Moreover these data underline the importance of beta-adrenergic agonists in surfactant metabolism.

The effects of intravascular application of endotoxin-depleted Escherichia coli hemolysin (HlyA) was studied in rabbits and monkeys. In rabbits, bolus application of HlyA calculated to effect final blood levels of approximately 2-3 HU/ml (200-300 ng/ml) caused an acute fall of polymorphonuclear blood leukocytes to less than 20% of starting levels within 5 min. Additionally, platelet counts dropped to approximately 30% of starting levels, whereas lymphocyte counts varied considerably and seldom fell to less than 50%. Nine out ten animals that received 2-4 HU/ml toxin died within 90 min post application. These animals presented with signs of acute respiratory failure and post mortem inspection of the internal organs revealed hemorrhagic pulmonary edema. Other internal organs appeared unaffected. Application of less than 1 HU/ml HlyA was never fatal (n = 9), and only transient leukopenia was noted. Monkeys presented with a remarkable and different response. Two animals were repeatedly given HlyA at high doses ranging from 3 to 10 HU/ml. Both animals developed selective granulocytopenia, but following a short, transient drop in blood pressure they showed no severe clinical signs of cardiovascular or pulmonary malfunction. Histological examinations revealed accumulation of polymorphonuclear granulocytes in both animals in liver, lung and spleen. Very high leukocyte elastase levels were measured in one animal over a period of 1.5 h. The present results demonstrate a remarkable tolerance of monkeys towards the leukocidal effects of E. coli hemolysin. Lethality in rabbits must be due to additional effects of the toxin, possibly on cells in the pulmonary vasculature. Neither pulmonary sequestration of granulocytes nor massive release of elastase from these cells is in itself sufficient to provoke pulmonary dysfunction in monkeys.

The major surfactant protein A (SP-A) determines the dynamics of surfactant metabolism and function. We now for the first time studied the in vivo exposure of the SP-A to nitrogen dioxide (NO2) and compared it to in vitro exposure effects. Several properties that are believed to possess physiological functions were investigated. Exposure of rat SP-A to NO2 showed 1) a higher alveolar pool size after in vivo exposure, 2) a slightly decreased mannose binding capacity for the in vivo exposed form but a highly decreased binding after in vitro exposure, 3) an affected protein-lipid aggregation that was impaired most by the in vitro exposed protein, 4) a low inhibition for the secretion of phosphatidylcholine in isolated type II pneumocytes, and 5) no difference in apparent molecular weight and immunological reactivity of the differently exposed SP-A. The NO2-induced alterations of the SP-A may contribute to the pulmonary toxicity of this oxidant. It is clear from this study that the extend of the effects from in vivo and in vitro exposure are different. Therefore both forms of exposure are necessary to assess the biological significance of NO2 exposure.

The lungs of 12 patients suffering from ARDS treated by ECCO2-R-therapy were examined. The thickness of the interlobular septa, area portions of honeycombing, bleeding and lung parenchyma with diffuse alveolar damage were assessed by semi-automatic image analysis. Medial thickness of the pulmonary arteries with an external radius ranging between 40 microns and 150 microns was assessed planimetrically. The area portion of honeycombing ranged from 0% to 66% (average: 28.8%, standard deviation: 17.0%). The thickness of interlobular septa was increased with values between 74.0 microns and 195.5 microns (average: 140.4 microns, standard deviation: 41.7 microns; normal controls: 72.0 microns +/- 19.5 microns). Parenchymal and vascular changes were closely related: Average medial thickness rose from nearly normal values (4.9%) in cases with low area portions of honeycombing and bleeding to the double (11.1%) of normal values in cases with area portions of honeycombing and bleeding greater than 40%. We conclude that parenchymal changes due to shock and high inspiratory O2 concentration lead to changes of the pulmonary arterial hemodynamics which result in a quickly developing medial hypertrophy.

Proteinase 3 (PR3), also referred to as myeloblastin, is a 26kD serine protease which is overexpressed in precursor cells of chronic myeloid leukaemia (CML). PR3 has previously been identified as the autoantigen of Wegener’s granulomatosis, which is characterized by a self-destructive humoral and T-cell response against PR3. However, high avidity PR3-specific cytotoxic T-cells (CTL) from CML patients specifically lysed CML blasts and their presence in vivo correlated with the achievement of a complete cytogenetic remission under interferon alpha (IFNα) therapy. Thus, overcoming tolerance to PR3 contributed to the elimination of leukaemia without causing auto-immunity (Molldrem et al., Nat. Med. 2000). We have previously shown that the induction of PR3 by IFNα in CD14+ monocytes may contribute to elicit a PR3-specific CTL expansion in CML. Since PR3-upregulation has subsequently been reported in monocytes of HIV- and pneumonia patients as well as in hepatitis C liver specimens, we asked, whether the upregulation of PR3 under inflammatory conditions may be linked to the expansion of PR3-specific T-cells. Therefore, we studied the frequency of PR3 specific CD8 positive CTL in patients with de novo diagnosed hepatitis C, a disease known to be associated with various autoimmune phenomenona. Thirty four HLA-A2.1 positive patients were analyzed by means of staining peripheral blood mononuclear cells using PR3-specific tetramers. 17 patients (50%) had PR3 specific CTL either at diagnosis (n=13) or developed them during follow up (n=4). Of the 13 patients, who had PR3-tetramer positive T-cells at diagnosis, six patients had both high and low aviditiy PR3-CTL, whereas seven patients had only low avidity PR3-specific T-cells. The frequency of these CD8 positive CTL at diagnosis ranged between 0.16% to 0.53% of all T-cells for the high avidity population and between 0.12 to 1.58% for the low avidity population. Upon antiviral therapy with IFNα and Ribaverin, the frequency of PR3-CTL became undetectable within less than 5 month of initiation of therapy in five of six patients of the high avidity PR3-CTL group. Only one patient of the patients with low avidity PR3-CTL at diagnosis was available for follow up testing and became negative. Interestingly, in four patients we saw a transient increase of low avidity PR3 specific CTL after initiation of therapy. Immunohistology of four hepatitis C liver sections and four healthy control specimens revealed a strong infiltration of PR3-overexpressing mononuclear cells in hepatitis liver, but PR3-negativity in normal livers. Hepatocytes did not express PR3. In conclusion: Hepatitis C is significantly associated with the induction of PR3-specific CTL and overexpression of PR3 in mononuclear cells may be important to drive their induction. PR3-specific CTL may be responsible for autoimmune phenomena in hepatitis C such as vasculitis and myelosuppression.

Slurry sampling in combination with ETV-ICP-AES was employed for the direct determination of trace amounts of impurities in silicon dioxide and silicon nitride. The ETV device consisted of a double layer tungsten coil in a quartz apparatus. Spectral interferences and background emission caused by tungsten ablation of the coil were reduced by coating the coil with tungsten carbide. The background was measured either with a high-purity sample, the suspension medium or close to the analyte emission line, depending on matrix and analyte, or it was calculated using relative emission intensities of tungsten. The concentrations of Al, B, Be, Ca, Cd, Co, Cr, Cu, Fe, Mg, Mn, Ni, Pb and Zn were measured simultaneously, whereas K and Na were determined in the sequential mode. Calibration was performed using the standard additions method. The accuracy was checked by comparison with the results of independent methods. Limits of detection between 0.035 (Mg) and 130 µg g–1 (B) and between 0.01 (Be, Mg) and 34 µg g–1 (B) were achieved in silicon dioxide and silicon nitride, respectively.