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A de Vries

Publications and source records attributed to A de Vries.

At least 73 records · Page 4Linked to original sources
PubMed1995

High-grade nucleoside transport inhibition stimulates ventilation in humans.

In 6 healthy male volunteers a placebo-controlled, double-blind, randomized, crossover trial was done to assess the effect of 1, 2, 4, and 6 mg of draflazine, a specific nucleoside transport inhibitor, on ventilation. Draflazine increased thoracic excursions dose-dependently by maximally (median with 95% confidence interval) 114.0% (38.3-184.8%) without affecting breathing rate. Ex vivo adenosine transport was inhibited by 0% (0-1%) after placebo, and 70% (59-74%), 81% (76-85%), 90% (86-93%), and 93% (90-96%) after the 4 increasing draflazine dosages, respectively (P < .05 for each draflazine dosage versus placebo). These results indicate that endogenously released adenosine may play a role in the regulation of ventilation.

Adenosine↗
PubMed1995

Frequent p53 alterations but low incidence of ras mutations in UV-B-induced skin tumors of hairless mice.

We have investigated UV-B-induced skin tumors of hairless SKH-HRA mice for alterations in the p53 gene and for mutations in either of the three ras genes. Out of 32 tumors screened, only one contained a ras mutation, i.e. in codon 12 of the K-ras gene. Alterations in the p53 gene were much more abundant, as illustrated immunohistochemically by the accumulation of p53 protein in 75% of the tumor sections examined. Immunoreactivity was observed primarily in the proliferative cell compartment, but no clear correlation between p53 staining in tumor cells and histological parameters for malignancy was observed. Subsequent sequence analysis showed that point mutations in the p53 gene are detectable in 30% (nine out of 30) of the skin tumors examined. The majority of the mutations are located in codons 267 and 272, most likely originating from UV-B-induced photo-adducts at dipyrimidine sites in the non-transcribed strand. Codon 272 corresponds to the human codon 278, which is also a hotspot for p53 mutations in human non-melanoma skin cancers. Codon 267 matches the human codon 273, which does not contain a dipyrimidine site, but represents a CpG hotspot for p53 mutations in internal malignancies. Our results demonstrate that this hairless mouse model for UV-induced skin cancer corresponds closely to human non-melanoma skin cancers with respect to mutations in the p53 gene.

Amino Acid Sequence↗
PubMed1995

The development of integrated service networks in Minnesota.

The formation of health insurance purchasing alliances in Minnesota has caused a restructuring of the provider system. One of the results has been the formation of competing delivery systems that organize hospitals, physicians, and insurance plans into vertically and horizontally integrated organizations termed integrated service networks (ISNs). This article describes the formation of these ISNs and identifies some of the salient features that distinguish them from other provider systems.

Capitation Fee↗
PubMed1994

Cloning and characterization of the mouse XPAC gene.

Xeroderma Pigmentosum is a human disease, which is, among others, characterized by a high incidence of (sunlight induced) skin cancer, due to a defect in nucleotide excision repair (NER). The human DNA repair gene XPAC corrects this defect in cells isolated from Xeroderma Pigmentosum complementation group A (XP-A) patients. To enable the development of a transgenic mouse model for XP-A by gene targeting in embryonic stem cells, we cloned and characterized the mouse homologue of the XPAC gene. The mouse XPAC gene was found to consist of 6 exons, spanning approximately 21 kb. The nucleotide sequence of the exons is identical to that of the also cloned the mouse XPAC cDNA. Furthermore, the deduced amino acid sequence of the XPAC protein is the same as the one published previously by Tanaka et al. From CAT assay analysis, the promoter of the XPAC gene appeared to be located within 313 bp upstream of the assumed transcriptional start site. Like the promoters of other eukaryotic DNA repair genes (i.e. ERCC-1 and XPBC/ERCC-3), the mouse XPAC promoter region lacks classical promoter elements like TATA-, GC- and CAAT boxes. However, it contains an unique polypyrimidine-rich box, which is so far only found in genes encoding DNA repair enzymes. The function of this box in the regulation of transcription is still unclear.

Animals↗
PubMed1994

The rat N-ras gene; interference of pseudogenes with the detection of activating point mutations.

The PCR technique in combination with selective hybridization to mutation specific oligonucleotides, is a widely used methodology for the detection of activating point mutations in ras oncogenes. In the present paper we demonstrate for the N-ras gene of the rat that processed pseudogenes do interfere with this method. A first indication for this interference came from the sequence analysis of cloned PCR fragments of exon 1, amplified with primers derived from previously reported exon sequences of the mouse N-ras gene. Between different clones originating from one PCR reaction, a marked sequence heterogeneity is observed and this is shown to be the result of the presence of at least two different processed pseudogenes of the rat N-ras gene. These two pseudogenes, together with the wildtype N-ras gene and a small 3' part of the unr gene, were eventually cloned and their genomic organization and nucleotide sequences determined. Furthermore, representative examples of the confounding effects of these pseudogenes on the screening for activating point mutations are presented. Taken together, our results demonstrate that intron-specific amplification is a prerequisite for the unambiguous detection of activating point mutations in the N-ras gene of the rat.

Amino Acid Sequence↗
PubMed1994

Comparison of two panels of monoclonal antibodies for determination of Chlamydia trachomatis serovars.

A panel of monoclonal antibodies was developed for serovar typing of clinical isolates of Chlamydia trachomatis. The panel could distinguish all 15 established serovars from one another, although the hybridomas of the panel were developed by fusions of myeloma cells and spleen cells from mice immunized with antigen derived from the urogenital serovars D to L3. The typing assay was based on a dot enzyme immunoassay, and the monoclonal antibodies that were included in the panel reacted strongly in this assay. A collection of 289 clinical isolates from The Netherlands was typed. The observed serovar frequency distribution was 51 isolates of serovar D (17.6%), 103 isolates of serovar E (35.6%), 62 isolates of serovar F (21.5%), 28 isolates of serovar G (9.9%), 14 isolates of serovar H (4.8%), 2 isolates of serovar I' (0.7%), 20 isolates of serovar J (6.9%), and 9 isolates of serovar K (3.1%). These results were confirmed by typing these isolates with a panel of monoclonal antibodies purchased from the Washington Research Foundation, Seattle. No strain variation was observed within serovar D with both panels. However, restriction fragment length polymorphism analysis of the gene encoding the major outer membrane protein showed that 32 isolates were similar to the prototype D and 17 were similar to the variant D-. The two others showed a new restriction pattern. Our panel of monoclonal antibodies contained one monoclonal antibody that divided the serovar G isolates into two groups. This differentiation was confirmed by restriction fragment length polymorphism analysis, confining this difference to a known sequence variation in variable domain IV. These data support the subdivision of serovar G into serovars G (prototype strain UW-57) and Ga (prototype strain IOL-238).

Animals↗
PubMed1994

Enzyme immunoassay with enhanced specificity for detection of antibodies to Chlamydia trachomatis.

Two different methods for preventing the binding of cross-reacting antibodies to the genus-reactive chlamydial lipopolysaccharide (LPS) were used to improve the specificity of an enzyme immunoassay for the determination of antibodies to Chlamydia trachomatis. Coated elementary bodies were treated with either sodium periodate, to oxidize the antigenic sites of the LPS, or Triton X-100, to extract the LPS. By using these new enzyme immunoassays, the standard enzyme immunoassay, and the whole inclusion fluorescence (WIF) assay, antibodies to C. trachomatis were determined in sera from different groups of patients and controls. Paired serum samples from patients with culture-proven urogenital C. trachomatis infections showed similar responses in all three assays. Paired serum samples from patients with Chlamydia psittaci infections showed similar responses in the WIF assay and the standard enzyme immunoassay, whereas significantly reduced titers were obtained in the enzyme immunoassays with treated antigen, especially in the convalescent-phase serum samples. Serum samples from patients with symptoms suggestive of infection with C. trachomatis, pregnant women, and blood donors were evaluated by all three types of assays. Eighty percent of the significant reductions in immunoglobulin G (IgG), IgA, and IgM titers were observed in sera with WIF assay titers in the lower classes (IgG, 1: < or = 256; IgA, 1: < or = 32; IgM, 1: < or = 16). From these results we conclude that oxidation of the antigen by sodium periodate is a simple and effective method of producing an enzyme immunoassay with enhanced specificity that could be useful for diagnostic purposes and seroepidemiological studies.

Acute Disease↗
PubMed1992

Efficacy of single-dose azithromycin versus doxycycline in the treatment of cervical infections caused by Chlamydia trachomatis.

The efficacy of single-dose azithromycin therapy in the treatment of cervical Chlamydia trachomatis infections was compared to that of a standard seven-day course of treatment with doxycycline. Cervical samples from 60 patients reacted positively in an enzyme immunoassay for detection of Chlamydia trachomatis. In 31 patients Chlamydia trachomatis was isolated from the sample taken before treatment. Fourteen of the 31 patients were treated with doxycycline and 17 with azithromycin. All cultures of samples taken one and four weeks after the start of therapy were negative. All 31 isolates showed a similar pattern of MICs for the seven antibiotics tested, including azithromycin and doxycycline. No differences were observed between isolates of different serovars. In samples from four patients chlamydial DNA could be detected by PCR one week after the start of the therapy and in two patients also after four weeks. No difference in microbiological parameters could be observed between the two treatment groups. It is concluded that single-dose azithromycin is as effective as a seven-day course of doxycycline in the therapy of cervical Chlamydia trachomatis infections.

Azithromycin↗
PubMed1990

Effect of cyclophosphamide pretreatment on daunorubicin in rat acute leukaemia model.

The total number of leukaemic cells at the time of therapy may affect the tissue and target cell distribution and antitumour efficacy of cytotoxic drugs. The effects of low dose cyclophosphamide pretreatment on daunorubicin concentrations in leukaemic bone marrow were investigated in rats. At day 12 after transplantation of the leukaemia, rats were injected intraperitoneally with cyclophosphamide (30 mg/kg). 2 days later the leukaemic rats received daunorubicin intravenously (7.5 mg/kg). Cyclophosphamide pretreatment led to a significant increase in daunorubicin concentration in the femoral bone marrow, by a factor of about 7. The log leukaemic stem cell kill (LCK) values, as estimated by a survival assay, were 1.8, 0.7, and 5.4 for the leukaemic rats injected with cyclophosphamide (day 12), with daunorubicin (day 14), or with cyclophosphamide (day 12) plus daunorubicin (day 14), respectively). The simultaneous administration of cyclophosphamide and daunorubicin at day 14, induced a LCK of 2.7, a value that was the sum of the LCKs of cyclophosphamide and daunorubicin alone. Low-dose cyclophosphamide pretreatment led to an increased daunorubicin accumulation in femoral bone marrow of leukaemic rats, and was synergistic with daunorubicin.

Animals↗
PubMed1989

Sampling intervals for clinical monitoring of variables during anesthesia.

Although five minutes is the sampling interval mentioned by the American Society of Anesthesiologists for monitoring blood pressure and heart rate during anesthesia, most patients are monitored more closely by continuous auscultation and with the help of automated instruments. Yet this difference between the interval recommended and that actually used indicates that sampling intervals are not defined clearly enough. Therefore, we present three methods with which to determine sampling intervals during monitoring. To explore the feasibility of these methods we examined data gathered every 7.5 seconds during three typical, noncatastrophic physiologic perturbations induced in an anesthetized dog. We chose hypercapnia secondary to rebreathing, hypotension secondary to deep anesthesia, and hypoxemia secondary to a low concentration of inspired oxygen as realistic examples of what can occur during operation and anesthesia. We studied three variables: respired carbon dioxide, femoral arterial blood pressure, and oxygen saturation of hemoglobin (pulse oximeter). The data obtained during monitoring were subjected to three methods of analysis: (1) recording of sets of data, with various starting times, at five-minute intervals only (moving grid); (2) Fourier analysis; and (3) analysis of slopes. For the data of the experiment, the Fourier analysis yielded, on average, longer sampling intervals than did the analysis of slopes.

Anesthesia, General↗
PubMed1987

Detection of activation of the contact system of coagulation in vitro and in vivo: quantitation of activated Hageman factor-C-1-inhibitor and kallikrein-C-1-inhibitor complexes by specific radioimmunoassays.

Radioimmunoassays (RIAs) for the detection of C-1-inhibitor (C-1-Inh) complexed to either kallikrein or activated Hageman factor (factor XIIa) are described. Kallikrein-C-1-Inh or factor XIIa-C-1-Inh complexes were bound to Sepharose to which monospecific antibodies against (pre)kallikrein or factor XII, respectively, were coupled. Bound complexes were subsequently detected by an incubation with affinity purified 125I-labeled antibodies against C-1-Inh. These RIAs were used to detect activation of the contact system of coagulation in vitro and in vivo. Addition of dextran sulfate (DXS) (20 micrograms/ml) to fresh plasma resulted at 37 degrees C in the rapid generation of amidolytic kallikrein activity, which was maximal after 1 to 2 min of incubation and subsequently decreased within a few minutes. The generation of kallikrein activity coincided with the appearance of both kallikrein-C-1-Inh and factor XIIa-C-1-Inh complexes. However, in contrast to kallikrein activity, both types of complexes remained detectable in the incubation mixtures during the incubation period. Experiments with purified kallikrein. C-1-Inh and partly purified beta-factor XIIa, and activation experiments in plasmas deficient in either factor XII or prekallikrein, demonstrated the specificity of both RIAs. The minimal amount of DXS that resulted in the generation of measurable amounts of both types of complexes in plasma was 2-3 micrograms per ml. Similar experiments with kaolin showed that with limiting amounts of activator (1-2 mg/ml), only kallikrein-C-1-Inh complexes were detected in plasma. When larger amounts of kaolin were added to plasma, factor XIIa-C-1-Inh complexes were additionally detected in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗