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M Jaspers

Publications and source records attributed to M Jaspers.

At least 19 recordsLinked to original sources

Integrated municipal solid waste treatment using a grate furnace incinerator: the Indaver case.

An integrated installation for treatment of municipal solid waste and comparable waste from industrial origin is described. It consists of three grate furnace lines with flue gas treatment by half-wet scrubbing followed by wet scrubbing, and an installation for wet treatment of bottom ash. It is demonstrated that this integrated installation combines high recovery of energy (40.8% net) with high materials recovery. The following fractions were obtained after wet treatment of the bottom ash: ferrous metals, non-ferrous metals, three granulate fractions with different particle sizes, and sludge. The ferrous and non-ferrous metal fractions can both be recycled as high quality raw materials; the two larger particle size particle fractions can be applied as secondary raw materials in building applications; the sand fraction can be used for applications on a landfill; and the sludge is landfilled. For all components of interest, emissions to air are below the limit values. The integrated grate furnace installation is characterised by zero wastewater discharge and high occupational safety. Moreover, with the considered installation, major pollutants, such as PCDD/PCDF, Hg and iodine-136 are to a large extent removed from the environment and concentrated in a small residual waste stream (flue gas cleaning residue), which can be landfilled after stabilisation.

Air Pollutants↗

Effect of improving flue gas cleaning on characteristics and immobilisation of APC residues from MSW incineration.

The flue gas cleaning system of a MSW incinerator with a capacity of 350 kt/year was changed to improve the HCl elimination efficiency. Instead of the semi-wet operating spray reactor and subsequent baghouse, a two-step wet flue gas cleaning was added behind the baghouse. Elemental composition, X-ray powder diffraction patterns and TGA measurements showed that the resulting APC residue was totally different from the former residue. As a consequence, leaching characteristics of both residues also differed and another treatment was required prior to disposal. For the former residue, mainly leaching of Pb (>100 mg/l), necessitated treatment prior to landfilling. The lower alkalinity of the new residue resulted in a leachate pH of 9.7 and a Pb concentration of 0.8 mg/l. The leachate pH of the former residue was 12.4. The leaching of Pb and Zn increased above 100 mg/l when immobilising the new residue with cement. Better results were obtained when immobilising with micro silica. The high CaCl2 x 2H2O content of the new residue brought along clogging of the bag filter system. Adding 1.4% of CaO (or 1.9% of Ca(OH)2) to the residue already improved these inconveniences but again significantly changed the leaching behaviour of the residue.

Calcium Carbonate↗

Carbonation of MSWI-bottom ash to decrease heavy metal leaching, in view of recycling.

The 0.1-2 mm fraction of a MSWI-bottom ash cannot be used as granular construction material because leaching of Cu exceeds Flemish limit values. In addition, leaching of Ba, Mo and Sb exceeds informal limit values. Leaching characteristics thus need to be improved. Carbonation was the chosen treatment method and this was performed by placing samples in a CO2 chamber. The CO2 percentage and the temperature of the chamber atmosphere, as well as the initial humidity of the samples, were varied to optimize carbonation parameters. Metal leaching was tested with the EN 12457 extraction test. Carbonation decreased Cu leaching from 3.3 to 1.0 mg/kg, but not yet to below the official limit value of 0.5 mg/kg. Leaching of Mo and Sb remained fairly constant or even increased after carbonation, but their limit values are only informal. Ba leaching decreased to below the informal limit value. Carbonation also caused Cr leaching to increase, in some cases to above the official limit value. Of the tested parameters, a CO2 percentage of 10% and a carbonation temperature of 50 degrees C in the atmosphere, together with ash humidity between 13% and 25% appeared to give the best leaching results. The main carbonation reactions took place within the first 24 h.

Carbon↗

Management of incinerator residues in Flanders (Belgium) and in neighbouring countries. A comparison.

This paper covers the Flemish legislative tools concerning the management of bottom ash, fly ash and APC residue from municipal waste incinerators, with respect to their contamination with heavy metals. The situation in Flanders is compared to the one in the Walloon region, The Netherlands, Germany and France. Waste management in the countries considered differs on the level of available management options, of leaching tests and of limit values. To make an indicative comparison of leaching tests and limit values in the different countries, leaching tests were carried out on bottom ash and fly ash, and the results are compared to the relevant limit values for recycling and landfilling of the different countries. The comparison of legislations as well as the leaching results show that discrepancies in waste management between the different regions and countries exist. Recently, European limit values for landfilling became available. European legislation on recycling, however, has not been developed and urgently needs to be considered and drafted as the market for recycling can be expanding rapidly.

Belgium↗

Comparison of immobilisation of air pollution control residues with cement and with silica.

Cement as agent for immobilising Pb from air pollution control residues is compared with the use of different silica-containing materials. The DIN 38414-S4 leaching test was used to control Pb leachability and to compare obtained Pb leachate concentrations with the landfill limit of 2 mg/l for Pb. Firstly, one scrubber residues was treated with cement and micro-silica. With cement, the Pb leachability could be reduced with a factor ranging from 3 to 50 depending on the type and amount of cement used and depending on the curing time. The landfill limit of 2 mg/l was, however, never attained. From all tested silica-containing additives, aerosil could reduce the initial Pb leaching (101.3mg/l) to below the detection limit at a dosage of 0.13 g aerosil/g residue. Second best and an economically preferable silica-containing additive was micro-silica: a reduction from 101.3 to 0.7 mg/l was observed at a dosage of 0.4 g micro-silica/g residue. The formation of Ca-silicates was found to be responsible for the decreased Pb leachability. To generalise the findings, the Pb leachability of five cement-treated and five micro-silica-treated air pollution control residues were compared. For three scrubber residues, 2-20 times lower Pb leachate concentrations were measured for micro-silica-treated samples (cured for 5 weeks) than cement-treated samples. For a fly ash and a boiler ash the difference was, respectively, 48 and 17 times. pH-dependent leaching tests showed that at pH=2.5, Pb leaching is 250 times lower for the micro-silica-treated residue than for the cement-treated residue and almost seven times lower at pH 12.4.

Air Pollutants↗

International Master Classes in health informatics.

Master Classes arose within the performing arts and are now being offered in system sciences. The IPhiE group of faculty from six universities in Europe and the United States has offered Master Classes in health informatics to provide an integrative forum for honors students. Featured are international views of health systems, varied opportunities for student interaction and promotion of informatics professionalism. Five years of experience indicate the success of this concept and suggest changes that will be considered for the future.

Curriculum↗

Immobilization of lead and zinc in scrubber residues from MSW combustion using soluble phosphates.

The immobilization of MSWI-scrubber residues with soluble PO4(3-) was studied and compared to the immobilization using cement. The DIN 38414-S4 leaching protocol and pH dependent leaching were used to evaluate the leaching of Pb and Zn. Four different scrubber residues from MSW combustion (Pb concentration: 2.8-4.8 mg/g; Zn concentration: 3.0-12.3 mg/g) were mixed with water and cement or Na2HPO4 as source of soluble PO4(3-) at dosages of at least 0, 0.1, 0.2, 0.3 and 0.4 g per g residue. With cement as well as with PO4(3-) a reduction in Pb and Zn leaching was observed. With 0.4 g cement per g residue, the Pb leaching was reduced by a factor ranging from 70 to 100, but still exceeded the Pb landfill limit of 2 mg/l. With PO4(3-) the Pb leaching was reduced with a factor of 100-300 to below 2 mg/l. The Zn landfill limit (10 mg/l) was only exceeded by one untreated residue. Adding 0.2 g cement or 0.1 g PO4(3-) per g of that residue was enough to reduce leaching below 10 mg/l. However, when 0.6 g Na2HPO4 per g residue was added to a lime based scrubber residue, an increase in Zn leaching up to 12.5 mg/l was observed due to an increase in pH of up to 13.0. When using NaH2PO4 and H3PO4 no such increase in Zn leaching was observed. pH dependent leaching performed on one of the four residues showed that in the pH range of 2.5-6, Pb leaching was 100-50 times lower with Na2HPO4 treatment than with cement. In the pH range from 7-11, almost equal results were obtained for cement treated and Na2HPO4 treated residue. Above a pH of 12, Pb leaching was three times lower for the PO(4)(3-)-treated residue than for the cement treated residue. With soluble PO4(3-), Pb leaching below 2 mg/l could be attained at a dosage of 0.27 g PO4(3-)/g residue. With cement, Pb leaching was never below 2 mg/l.

Belgium↗

Genotype/phenotype correlation of the G85E mutation in a large cohort of cystic fibrosis patients.

In this European study, the phenotype in 68 patients, homozygous or compound heterozygous for the G85E mutation, was investigated. Each index case was compared with two cystic fibrosis (CF) patients from the same clinic, matched for age and sex: one with pancreatic sufficiency (PS) and one with pancreatic insufficiency (PI). When comparing 31 G85E/F508del and F508del/F508del patients, there were no differences in median age at diagnosis, mean sweat chloride value, most recent weight for height, most recent forced expiratory volume in one second % predicted, prevalence of chronic Pseudomonas aeruginosa colonisation and typical CF complications. However, PI was less frequent in the G85E/F508del group. Comparison of 55 G85E patients (with second mutation known and not classified as mild) with PS controls (n=44) showed that the G85E patients had a significantly higher sweat chloride, more often failure to thrive at diagnosis, higher prevalence of PI, worse current weight for height, higher prevalence of chronic P. aeruginosa colonisation and liver cirrhosis. Pulse-chase experiments revealed that G85E cystic fibrosis transmembrane conductance regulator failed to mature on a M470 as well as on a V470 background. Therefore, G85E is a class II mutation. Although there is variability in its clinical presentation, G85E mutation results in a severe phenotype.

Adolescent↗

Functional interaction between TRP4 and CFTR in mouse aorta endothelial cells.

BACKGROUND: This study describes the functional interaction between the putative Ca2+ channel TRP4 and the cystic fibrosis transmembrane conductance regulator, CFTR, in mouse aorta endothelium (MAEC). RESULTS: MAEC cells express CFTR transcripts as shown by RT-PCR analysis. Application of a phosphorylating cocktail activated a Cl- current with characteristics similar to those of CFTR mediated currents in other cells types (slow activation by cAMP, absence of rectification, block by glibenclamide). The current is present in trp4 +/+ MAEC, but not in trp4 -/- cells, although the expression of CFTR seems unchanged in the trp4 deficient cells as judged from RT-PCR analysis. CONCLUSIONS: It is concluded that TRP4 is necessary for CFTR activation in endothelium, possibly by providing a scaffold for the formation of functional CFTR channels.

Animals↗

Suppressive interactions between mutations located in the two nucleotide binding domains of CFTR.

The S1235R locus in CFTR was studied in combination with alleles found at the M470V and G628R loci. While R628 caused a maturational defect, R1235 did not. The impact of R1235 was found to be influenced by the alleles present at the G628R and M470V loci. At the single channel level, R1235-V (R1235 on a V470 background) was characterized by an open probability significantly higher than V470-wildtype CFTR. M470, which on its own increases CFTR chloride transport activity when compared to V470-wildtype CFTR, suppressed the activity of R1235 in such a way that a protein with an open probability not significantly different from V470-wildtype CFTR was obtained. While R628-V CFTR had similar current densities as V470-wildtype CFTR in Xenopus laevis oocytes, R1235-V resulted in current densities that were more than twofold higher than those of V470-wildtype CFTR. However, the current densities generated by R1235/R628-V (R1235 and R628 on a V470 background) CFTR were significant lower than R1235-V or R628-V CFTR.

Alleles↗

Functional characterization of the CFTR R domain using CFTR/MDR1 hybrid and deletion constructs.

To improve our insight into the structure and function of the CFTR R domain, deletion and hybrid constructs in which different parts of the R domain were deleted or replaced by the MDR1 linker domain, and vice versa, were made. Replacement of the linker domain by the R domain did not result in a decrease and replacement of the CFTR R domain by the linker domain did not result in an increase of maturation efficiency, when compared to the respective wild-type proteins. This indicates that the R domain is not responsible for the high degree of degradation observed for CFTR translation products in the ER, but rather the overall structure or sequences located outside the R domain. Replacing the C-terminal part of the R domain (amino acids 780-830) by the MDR1 linker domain resulted in the appearance of PKA-dependent whole cell chloride currents which were not significantly different from wild-type CFTR currents. This might indicate that the PKA sites present in the linker domain are functional and that not the exact sequence of the C-terminal part of the R domain is important, but rather the presence of PKA sites and the length. Moreover, when this hybrid construct was PKC-stimulated, chloride currents were activated. Although these PKC-induced currents were lower than the PKA-induced ones, this again indicates that the linker domain is functional in this hybrid construct. Taken together, these results suggest that the MDR1 linker domain can substitute for part of the regulatory domain of the CFTR protein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Mutation analysis in adenylosuccinate lyase deficiency: eight novel mutations in the re-evaluated full ADSL coding sequence.

The deficiency of adenylosuccinate lyase (ADSL, also termed adenylosuccinase) is an autosomal recessive disorder characterized by the accumulation in body fluids of succinylaminoimidazole-carboxamide riboside (SAICA-riboside) and succinyladenosine (S-Ado). Most ADSL-deficient children display marked psychomotor delay, often accompanied by epilepsy or autistic features, or both, although some patients may be less profoundly retarded. Occasionally, growth retardation and muscular wasting are also present. Up to now, nine missense mutations of the ADSL gene had been reported in six apparently unrelated sibships. In the present study of 10 additional patients with ADSL deficiency, nine point mutations, among which seven unreported missense mutations, and the first splicing error reported in this disorder, have been identified. These mutations have been characterized, taking into account the finding that the cDNA of human ADSL is 75 nucleotides longer at its 5'-end, and encodes a protein of 484 rather than 459 amino acids as previously reported. Five apparently unrelated patients were found to carry a R426H mutation. With the exceptions of the latter mutation, of a R190Q mutation that had been reported previously, and of a K246E mutation that was found in two unrelated patients, all other mutations were found only in a single family.

Adenylosuccinate Lyase↗

Characterization of mutations located in exon 18 of the CFTR gene.

In order to get a better insight into the function of amino acid residues located in the second transmembrane domain of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, all exon 18 mutations found in cystic fibrosis (CF) patients were characterized at the protein and at the electrophysiological level. Of the different mutations present in transmembrane helix 12 (M1137V, M1137R, I11139V and deltaM1140), and the intracytoplasmic loop connecting TM12 and NBD2 (D1152H and D1154G), only M1137R interfered with the proper maturation of the protein. Permeability studies performed after injection of the different wild-type and mutant cRNAs in Xenopus laevis oocytes indicated that the mutations did not alter the permeability sequence of the CFTR channels. The whole cell cAMP activated chloride currents, however, were significantly reduced for M1137V, I1139V, D1152H and D1154G and close to zero for deltaM1140, indicating that these mutations interfere with the proper gating of the chloride channels.

Animals↗

Polyvariant mutant cystic fibrosis transmembrane conductance regulator genes. The polymorphic (Tg)m locus explains the partial penetrance of the T5 polymorphism as a disease mutation.

In congenital bilateral absence of the vas deferens patients, the T5 allele at the polymorphic Tn locus in the CFTR (cystic fibrosis transmembrane conductance regulator) gene is a frequent disease mutation with incomplete penetrance. This T5 allele will result in a high proportion of CFTR transcripts that lack exon 9, whose translation products will not contribute to apical chloride channel activity. Besides the polymorphic Tn locus, more than 120 polymorphisms have been described in the CFTR gene. We hypothesized that the combination of particular alleles at several polymorphic loci might result in less functional or even insufficient CFTR protein. Analysis of three polymorphic loci with frequent alleles in the general population showed that, in addition to the known effect of the Tn locus, the quantity and quality of CFTR transcripts and/or proteins was affected by two other polymorphic loci: (TG)m and M470V. On a T7 background, the (TG)11 allele gave a 2.8-fold increase in the proportion of CFTR transcripts that lacked exon 9, and (TG)12 gave a sixfold increase, compared with the (TG)10 allele. T5 CFTR genes derived from patients were found to carry a high number of TG repeats, while T5 CFTR genes derived from healthy CF fathers harbored a low number of TG repeats. Moreover, it was found that M470 CFTR proteins matured more slowly, and that they had a 1.7-fold increased intrinsic chloride channel activity compared with V470 CFTR proteins, suggesting that the M470V locus might also play a role in the partial penetrance of T5 as a disease mutation. Such polyvariant mutant genes could explain why apparently normal CFTR genes cause disease. Moreover, they might be responsible for variation in the phenotypic expression of CFTR mutations, and be of relevance in other genetic diseases.

Alleles↗

Characterization of 19 disease-associated missense mutations in the regulatory domain of the cystic fibrosis transmembrane conductance regulator.

In order to gain a better insight into the structure and function of the regulatory domain (RD) of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, 19 RD missense mutations that had been identified in patients were functionally characterized. Nine of these (I601F, L610S, A613T, D614G, I618T, L619S, H620P, G628R and L633P) resulted in aberrant processing. No or a very small number of functional CFTR proteins will therefore appear at the cell membrane in cells expressing these mutants. These mutations were clustered in the N-terminal part of the RD, suggesting that this subdomain has a folding pattern that is very sensitive to amino acid changes. Mutations that caused no aberrant processing were further characterized at the electrophysiological level. First, they were studied at the whole cell level in Xenopus laevis oocytes. Mutants that induced a whole cell current that was significantly different from wild-type CFTR were subsequently analysed at the single channel level in COS1 cells transiently expressing the different mutant and wild-type proteins. Three mutant chloride channels, G622D, R792G and E822K CFTR, were characterized by significantly lower intrinsic chloride channel activities compared with wild-type CFTR. Two mutations, H620Q and A800G, resulted in increased intrinsic chloride transport activities. Finally, T665S and E826K CFTR had single channel properties not significantly different from wild-type CFTR.

Amino Acid Sequence↗

The genomic structure of the murine alpha 4 integrin gene.

The VLA-4 (alpha 4 beta 1) integrin is a leukocyte glycoprotein involved in both cell-extracellular matrix and cell-cell interactions. We report here the cloning of the murine alpha 4 gene whose protein product is antigenically related to the human VLA-4 alpha chain. The alpha 4 m gene is about 75 kb long and consists of 28 exons, ranging in size from 46 bp (exon 13) to 437 bp (exon 1). The introns varied from 79 bp (intron 8) to more than 17 kb (intron 2). Three mRNA transcripts from this alpha 4 m gene can be visualized on Northern blot. After cloning the 3' untranslated region (3' UTR), four polyadenylation sites could be identified, presumably responsible for the presence of three to four transcripts of the alpha 4 gene, differing substantially in length.

Animals↗

A 68-kD antigen, which is probably an N-terminal fragment of the VLA-5 alpha 5-subunit, is specific for differentiating keratinocytes.

BACKGROUND: During terminal differentiation, basal keratinocytes lose gradually contact with the basement membrane, a process accompanied by the progressive functional down-regulation and loss of integrin expression. Understanding the molecular nature of this complex mechanism will eventually lead to insight into the pathogenesis of differentiation disorders of the epidermis, e.g. psoriasis. OBJECTIVE: The monoclonal antibody 8D9 against the very late antigen 5 (VLA-5) integrin subunit was used to study the expression and down-regulation of this protein in several experimental paradigms of keratinocyte differentiation. METHODS: Primary cultures of human keratinocytes were prepared and used as such, or after induction of terminal differentiation with methylcellulose and/or calcium. Expression of the 8D9 epitope was analyzed using immunoblotting, protein chemistry and immunocytochemistry on cultured cells and on skin biopsies from control and psoriatic patients. RESULTS AND CONCLUSION: The monoclonal antibody 8D9 reacts with the alpha 5-subunit of human VLA-5 integrin and with a 68-kD antigen that is strongly expressed in differentiating keratinocytes in vitro and in the cornified layers of human skin in vivo. Psoriatic skin showed additional immunoreactivity in the upper spinous and granular layers. Based on indirect immunological and chemical evidence we suggest that the 68-kD protein is an amino-terminal degradation product of the alpha 5-subunit, which provides a new and interesting marker of differentiating keratinocytes.

Antibodies, Monoclonal↗