Childhood immunizations.
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Biomedical subjects
Publications and source records attributed to P Pohl.
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The irradiation of bilayer lipid membranes with continuous ultrasound of a frequency of 8.2 MHz and a spacial peak time average (SPTA) intensity of 0.4 W/cm2 reduces the thickness of the unstirred layer up to 40% of its initial value under our conditions. This result was obtained from measurements of the transmembrane potential which appears after the addition of a protonophore in the presence of a gradient of acetic acid. Ultrasound exposure decreases this potential when the pH of the buffer solutions is much higher than the pK of CH3COOH and has no effect at low pH values. The latter can be explained by a simultaneous increase of the permeability of acetic acid and the buffer substances, respectively, due to ultrasound irradiation.
A general statement about the driving ability of HIV-positive as well as HIV-negative addicts undergoing methadone-substitution treatment cannot be made with certainty. Even isolated observations are not significant; only an individually performed assessment, free of prejudice and conscientiously done is decisive. The formal assertion that addiction equals driving-inability, which is largely practised at present, is inadmissible and therefore harmful to the therapeutic efforts for rehabilitation.
This paper presents a simple model to describe experimental data on weak acid transport across planar bilayer lipid membrane separating two buffered solutions. The model takes into account multiple proton-transfer reactions occurring in the unstirred layers (ULs) adjacent to the membrane. Differential equations of the model are shown to be reduced to a set of nonlinear algebraic equations. Since the latter equations depend monotonically on unknown variables, they can be easily solved numerically, using bisection method. For the particular system studied experimentally (with acetate as the weak acid and TRIS+MES as the buffer mixture) pH profiles in the ULs are calculated from the model. These results are compared with experimental data obtained using pH microelectrode. The agreement between theoretical and experimental pH profiles is found to be satisfactory. The most pronounced deviations are observed at the UL/bulk solution boundary. To obtain a better correlation between the theoretical and experimental results, two other, less idealized models are considered. They take into account, respectively, (a) the electric field arising in the ULs from ion diffusion and (b) finiteness of the rates of proton-transfer reactions. However, both acetate membrane fluxes and pH profiles in the ULs computed from these models are found to be close to those of the simple model. One can thus conclude that the difference between experimental and theoretical pH profiles is due to the inconsistency of the generally accepted model of the "unstirred layer", assuming the existence of a strict boundary between the regions of "pure diffusion" and "ideal stirring".
Colonization of the small intestine and the excretion of a toxin are important steps in the pathogenesis of edema disease in pigs. Although much is known about the chemical and biological characteristics of SLT-IIv toxin, its mode of action and its genetic determinant, F107 fimbriae were only recently described as colonization factors. Here we summarize our current knowledge about the virulence factors F107 fimbriae and SLT-IIv toxin.
Escherichia coli and salmonella strains with plasmids conferring resistance to gentamicin and apramycin have been isolated with increasing frequency both from cattle and hospital patients in Belgium. The apramycin-gentamicin resistance plasmids were characterized in recipient strains by their profiles and molecular weights using agarose gel electrophoresis, by their antimicrobial resistance patterns and by replicon typing using a series of DNA probes specific for the genes controlling their systems of replication. Overall, most of the plasmids differed in their DNA electrophoretic patterns. Seventeen different antimicrobial resistance profiles were observed, and there were six different types of replicons. However, two replication genes predominated and had a preferential distribution in different bacterial species. The rep FIC.a plus rep Q multireplicon was found mainly in plasmids recovered from gentamicin- and apramycin-resistant E. coli while replicon of the type rep FIC.b largely prevailed in S. typhimurium. Identical replication genes were found in most animal and human strains, hence suggesting a high homology between apramycin-gentamicin plasmids in these communities. Finally, our results indicate that the rapid spread of apramycin-gentamicin-resistance in several species of Enterobacteriaceae isolated from animals and from humans in Belgium is not due to a single plasmid, but rather that the gene encoding AAC(3)-IV is carried by various replicons.
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Two DNA probes were used for the detection of CNF1- and CNF2-positive E coli strains in a collection of 553 E coli isolates from cattle, sheep, goats, pigs, horses, dogs, cats and poultry. CNF-positive E coli were frequently associated with septicaemia in cattle, dogs, and cats, with diarrhoea in calves, cats and dogs, and with abortion in bovine and porcine species. CNF2-positive strains were observed among adult healthy cattle. They were also found in cases of pneumonia, metritis, mastitis in cattle and in 1 case of metritis of a mare. The physiopathology induced by CNF-positive E coli strains remains to be elucidated. However, the impact of CNF strains on veterinary pathology is clear and the diagnosis of CNF-producing E coli should become routine in veterinary practice.
We present a case-report and review of the literature on membranous lipodystrophy. This is a rare disease characterized by progressive presenile dementia, multiple bone cysts with pathologic fractures, generalized cerebral seizures with abnormal EEG and bilateral calcifications of the basal ganglia. Neuropathological findings are neuroaxonal dystrophy with neurofilaments in the axons, neuronal cell loss and fibrillary gliosis. The disease is usually inherited as an autosomal recessive. The pathogenesis is unknown but is believed to be an enzyme defect of the glycolipid metabolism.
F107 fimbriae were isolated and purified from edema disease strain 107/86 of Escherichia coli. Plasmid pIH120 was constructed, which contains the gene cluster that codes for adhesive F107 fimbriae. The major fimbrial subunit gene, fedA, was sequenced. An open reading frame that codes for a protein with 170 amino acids, including a 21-amino-acid signal peptide, was found. The protein without the signal sequence has a calculated molecular mass of 15,099 Da. Construction of a nonsense mutation in the open reading frame of fedA abolished both fimbrial expression and the capacity to adhere to isolated porcine intestinal villi. In a screening of 28 reference edema disease strains and isolates from clinically ill piglets, fedA was detected in 24 cases (85.7%). In 20 (83.3%) of these 24 strains, fedA was found in association with Shiga-like toxin II variant genes, coding for the toxin that is characteristic for edema disease strains of E. coli. The fimbrial subunit gene was not detected in enterotoxigenic E. coli strains. Because of the capacity of E. coli HB101(pIH120) transformants to adhere to isolated porcine intestinal villi, the high prevalence of fedA in edema disease strains, and the high correlation with the Shiga-like toxin II variant toxin-encoding genes, we suggest that F107 fimbriae are an important virulence factor in edema disease strains of E. coli.
We measured in simultaneously withdrawn cerebrospinal fluid (CSF) and serum samples from 56 endocrinologically grossly normal patients the concentrations of several lipophilic unconjugated steroids [i.e. dehydroepiandrosterone (DHEA), androstenedione, cortisol, progesterone, testosterone] and their hydrophilic counterparts, i.e. DHEA-sulfate, or hydrophilic binding proteins, i.e. albumin, sex hormone-binding globulin (SHBG) and corticosterone-binding globulin (CBG). CSF levels of total (i.e. free plus protein-bound) DHEA, androstenedione, cortisol, progesterone, and testosterone were found to be in the 0.02-2 nM range and only cortisol reached levels approximately 20 nM. These values were of the same order of magnitude as the reported and calculated free serum levels of these steroids. In patients with disturbed (abnormally leaky) blood-CSF barrier (BCB) function, CSF levels of these steroids were not different from those with intact BCB, in contrast to DHEA-sulfate, CBG and SHBG whose CSF levels were significantly elevated, that is similar (i.e. 2-5) fold as those of albumin. In vitro demonstrated low affinity (micromolar) interactions of steroids with neuronal membrane-bound neurotransmitter receptors should be considered in perspective to the here reported finding that steroids occur in vivo at best in nanomolar concentrations in the CSF. Whether in other extracellular fluid compartments of the brain higher levels of steroids than in CSF can accumulate is as yet not clear. Very probably, pathological production or excessive dosage of steroids that are negligibly bound to SHBG or CBG will produce CSF and brain levels in the near micromolar range.
Virulence factors and phenotypes of 61 strains CNF1+ were investigated. Eighty-nine percent of the strains produced an aerobactin and were resistant to the bactericidal activity of sheep serum, both of which are properties of septicemic strains of E coli. None of the strains reacted either with DNA probes corresponding to the enterotoxins STaP, STb, LT-I and LT-IIa, or to the verotoxins VT-I and VT-II. None produced the adhesins K99, Att25 (FY or F17) and Att111. The great majority (93.4%) of the CNF1+E coli possessed both properties. These properties allow CNF1+ to be distinguished from CNF-E coli.
Single photon emission computed tomography (SPECT) using N-isopropyl-p-(123I)iodoamphetamine (123I-IMP) and 99Tcm-hexamethylpropyleneamine oxime (99Tcm-HMPAO) was performed in 25 patients with different clinical stages of AIDS encephalopathy. The average interval between the two examinations was 7 days. In 15 of the 25 cases (60%) 99Tcm-HMPAO scans were different from 123I-IMP scans. Uptake defects of different extent were observed in 8 of 25 cases (32%), of different extent and different location in 3 of 25 cases (12%) and of identical extent but of different location in 4 of 25 cases (16%). Differences in the uptake patterns of 123I-IMP and 99Tcm-HMPAO with regard to extent and/or location were more commonly shown in patients with early acquired immunodeficiency syndrome (AIDS) encephalopathy (P = 0.0372). In this group, 99Tcm-HMPAO showed uptake defects of greater extent more frequently than did 123I-IMP (P = 0.0156). Our data indicate different brain uptake mechanisms of 123I-IMP and 99Tcm-HMPAO in early and advanced AIDS encephalopathy.
We studied 41 AIDS patients in the Austrian Tyrol with respect to toxoplasma antibody titers and the presence of CNS toxoplasmosis. In no patient had primary Pneumocystis carinii pneumonia (PcP) prophylaxis with either trimethoprim/sulfamethoxazole or pyrimethamine/sulfadoxine been applied; the degree to which CNS toxoplasmosis is influenced by this kind of PcP chemoprophylaxis, widely used elsewhere, is still unclear. In this study 47.4% of toxoplasma-seropositive patients developed CNS toxoplasmosis, compared to the previously estimated risk of 12%-28% for developing CNS involvement in such patients. In view of the high risk of toxoplasma-seropositive patients with AIDS, increased efforts in developing a well-tolerated chemoprophylaxis to combat CNS toxoplasmosis are required.
Since 1987, the number of cases of salmonellosis caused by Salmonella enteritidis has considerably increased in Western Europe. Comparison of endemic animal strains isolated in Belgium from 1976-84 with strains isolated from 1987 on shows that the strains which cause the current epidemic have no features distinguishing them from the previously-isolated strains and that furthermore, they do not constitute a bacterial clone. They belong to 13 different lysotypes and in most cases remain sensitive to antibiotics. Nevertheless, the lysotype 33 (which belongs to the phage type 4 has increased significantly. It encompasses 37% of the animal strains isolated in Belgium from 1987-9, but only 7% of the strains isolated from 1976-84. It is worth noting that the endemic as well as the epidemic strains contain a virulence plasmid sharing sequence similarities with the FIB and FIIA plasmid replicons and with the VirA and VirB virulence regions of the S. typhimurium virulent plasmid: pIP1350.
Escherichia coli and Salmonella strains resistant to gentamicin and apramycin were isolated from cattle in France and Belgium and from patients in hospitals. Homology between plasmids of both human and animal origins encoding aminoglycoside 3-N-acetyltransferase was revealed by digestion with several restriction endonucleases and confirmed by hybridization with different replicon-specific probes.
Enterotoxigenic Escherichia coli strains express fimbriae which mediate binding to intestinal mucosal cells. The F17 fimbriae mediate binding to N-acetylglucosamine-containing receptors present on calf intestinal mucosal cells. These fimbriae consist of F17-A subunit peptides. Analysis of the F17 gene cluster indicated that at least the F17-A, F17-C, F17-D, and F17-G genes are indispensable to obtain adhesive F17 fimbriae (unpublished data). Genetic evidence is presented that the F17-G protein, a minor fimbrial component, is required for the binding of the F17 fimbriae to the intestinal villi. The F17-G gene was cloned and sequenced. An open reading frame of 1,032 bp encoding a polypeptide of 344 amino acids, starting with a signal sequence of 22 residues, was localized. The F17-G mutant strain produced F17 fimbriae which were morphologically identical to the fimbriae purified from strains which contained the intact F17 gene cluster. However, this F17-G mutant could no longer adhere to calf villi. The F17-G locus was shown to act in trans: transformation of the F17-G mutant strain, still expressing the genes F17-A, F17-C, and F17-D, with a vector expressing the F17-G gene restored the binding activity of this mutant strain.
Forty-three bovine isolates of Escherichia coli producing a second type of cytotoxic necrotizing factor (CNF2) and three K-12 strains carrying different Vir plasmids coding for CNF2 were tested for the presence of several virulence factors. Most of the strains were serum resistant (79%), produced an aerobactin (70%), and adhered to calf villi (53%); some of them produced a colicin (32%) and a hemolysin (9%). These strains were also tested by a colony hybridization assay with gene probes for six toxins (classical heat-stable [STaP and STb] and heat-labile [LT-I and LT-IIa] enterotoxins and Shiga-like toxins [SLT-I and SLT-II]) and five adhesion factors (K99, K88, 987P, F17, and F41). Only two gene probes, LT-IIa (9%) and F17A (53%), hybridized with the CNF2 strains. However, antibodies raised against F17 fimbriae did not agglutinate the strains hybridizing with the F17A probe. In contrast, all except one of these strains adhered to calf villi. Interestingly, these two properties, F17A positivity and adherence to calf villi, were the only ones expressed by the K-12 strains carrying different Vir plasmids. In conclusion, this study confirmed that CNF2-producing strains are unrelated to previously described toxigenic E. coli strains and also demonstrated that in half of the strains the production of CNF2 was associated with an adhesion factor genetically related to, but different from, F17, which is more than likely encoded by Vir plasmids.