Search PubMed⌕ Search

Biomedical subjects

J De Vries

Publications and source records attributed to J De Vries.

At least 37 records · Page 2Linked to original sources

Serum beta-glucuronidase activity in a population of ex-coalminers.

BACKGROUND: The aim of this study was to investigate whether BGD activity is of additional value in the assessment of pulmonary inflammation caused by coal dust exposure. DESIGN AND METHODS: Ex-coalminers were included in this study. Forty-eight healthy male subjects, without a relevant medical history, were used as controls. RESULTS: In ex-coalminers serum BGD activity was higher compared to the control group. Moreover, ex-coalminers with a normal chest radiograph and normal serum LDH demonstrated elevated serum BGD compared to the control group. However, no relation was found in the total group of ex-coalminers between serum BGD activity and pulmonary function parameters. CONCLUSIONS: Our study adds in vivo human evidence to the already existing animal data that BGD is a potential biomarker useful in monitoring pulmonary inflammation caused by coal dust exposure.

Aged↗

Impairment of quality of life: rheumatoid arthritis versus sarcoidosis.

BACKGROUND: Quality of life (QOL) has become an important item in health care. QOL should be a major target of treatment in chronic diseases such as rheumatoid arthritis (RA) and sarcoidosis. The aim of this study was to compare the impact of RA and sarcoidosis on patients' QOL. We expected more serious impairment of QOL in the RA group than in the sarcoidosis group. METHODS: QOL was studied in RA patients (n = 32), sarcoidosis patients (n = 37), and a healthy control group (n = 37) employing the World Health Organization Quality of Life assessment instrument (WHOQOL-100). RESULTS: In both patient groups QOL was impaired with respect to Physical Health, Level of Independence (P < 0.001), and Overall QOL and General Health (P < 0.01). Moreover, RA patients appeared to have a lower QOL with respect to Pain and Discomfort (P < 0.001) and Mobility (P < 0.001). CONCLUSIONS: In RA and sarcoidosis, fatigue and sleep were major problems. In contrast to our expectations, with respect to activities of daily living and working capacity, the two patient groups did not show any difference. Impairment of QOL was more serious and included more aspects of QOL in RA than in sarcoidosis.

Adult↗

Gender differences in sarcoidosis: symptoms, quality of life, and medical consumption.

The aim of this study was to examine gender differences in quality of life (QOL) and in constitutional symptoms that coincide with sarcoidosis. The study population included 1026 sarcoidosis patients--all members of the Dutch Sarcoidosis Society--who completed the WHOQOL-100 and a symptom checklist. Women experienced more symptoms than men. With regard to QOL, male and female patients who suffered from symptoms differed in the broader domains of Physical Health and Psychological Health. Specific facets reflected pain, sleep, positive affect, appearance, mobility, and activities of daily living. Future studies should focus on the different experience of the disease between male and female patients more extensively. Studies are needed to evaluate whether the differences in the present study between male and female sarcoidosis patients are caused by a subject selection bias or life style differences; have a genetic, hormonal or biological base; or just are an epiphenomenon.

Adaptation, Physiological↗

Quality of life in sarcoidosis: a comparison between members of a patient organisation and a random sample.

UNLABELLED: BACKGROUND AND AIMS OF THE WORK: Although it often has been suggested that members of patient organisations concerning a particular disease might not be representative of patients with that particular disease in general, this hypothesis has not been tested. Therefore, the aim of this study was to evaluate whether the quality of life (QOL) of members of the Dutch Sarcoidosis Society (DSS) is comparable with the QOL of a random non-member sample of the Dutch sarcoidosis population. SUBJECTS AND METHODS: The study included 64 out-patients (Group I), 192 DSS members matched for age and gender (Group II), and 192 DSS members matched for age, gender, as well as symptoms (Group III). All subjects filled in a questionnaire to make an inventory of physical symptoms and the World Health Organization Quality of Life assessment instrument (WHOQOL-100). The Student's t-test was used to evaluate the differences between (i) the two DSS groups and (ii) the non-member group. RESULTS: Group III differed significantly from Group I in only one QOL domain and five facets. Moreover, considering only the patients with symptoms from Group I and Group III, differences emerged on one domain and two facets. CONCLUSIONS: It appeared that more members of the DSS declared they suffered from physical symptoms than non-members. When the experience of symptoms was partialled out fewer QOL differences remained.

Adult↗

The single-stranded-DNA-binding proteins (SSB) of Proteus mirabilis and Serratia marcescens.

The single-stranded-DNA-binding (SSB) proteins from Proteus mirabilis and Serratia marcescens were purified from overproducing Escherichia coli strains, which were devoid of their own ssb gene. The strains harboured an endA insertion mutation and a xonA mutation resulting in the absence of endonuclease I and exonuclease I activities from the preparations. The amino acid sequences of the SSB of all three species are nearly identical in the N-terminal parts of the proteins that contain the DNA-binding domain, but differ in the C-terminal parts. Both proteins have an apparent binding-site size of 65 and 35 nucleotides at high and low salt concentrations, respectively. The association-rate constant for binding to poly(dT) is 3.2 x 10(8) M-1 s-1 for P. mirabilis SSB (PmiSSB) and 3.4 x 10(8) M-1 s-1 for S. marcescens SSB (SmaSSB). These binding parameters are very similar to those of E. coli SSB (EcoSSB). The structural similarity of the proteins is also documented by the finding that they can exchange subunits among each other to form mixed tetramers. The transcriptional regulation of the ssb and uvrA genes from P. mirabilis and S. marcescens in SOS-induced E. coli cells was studied using lacZ fusions. While the uvrA genes were inducible, there was no induction of the ssb genes transcribed divergently from the uvrA genes. Apparently, regions with nucleotide sequence similarity to the E. coli SOS-box preceding the ssb genes of P. mirabilis and S. marcescens had no gross effect on the transcription. Studies on growth of the cells and recovery from ultraviolet damage indicate that the heterologous SSB proteins support DNA replication and recombinational DNA repair of E. coli with the same efficiency as the E. coli SSB protein. Interactions with other E. coli proteins involved in these processes either do not occur, or are not impeded.

Amino Acid Sequence↗

Patterns of body temperature during feeding in rats under varying ambient temperatures.

Relationships between feeding and body temperature of rats were investigated at three ambient temperatures during the whole light/dark cycle. Basal liver temperature was negatively correlated with ambient temperature. Only at 29 degrees C liver temperature indicated activation of autonomic and locomotory thermoregulatory responses due to heat stress. At 21 degrees C, liver temperature was always higher than skin temperature. Both showed a clear circadian rhythm with higher values during the dark phase. Meal-associated temperature patterns were superimposed on this circadian rhythm. Liver and skin temperatures showed a preprandial and prandial rise. Liver temperature reached an almost similar peak value just above 39 degrees C at the end of a meal, irrespective of meal size and ambient temperatures of 13 degrees C and 21 degrees C. Liver temperature reached this peak about 2 min earlier and dropped sooner than skin temperature. These results indicate a threshold liver temperature at which feeding activity stops. The present study suggests that temperatures do not exceed this value by adaptive autonomic thermoregulatory responses shifting heat flow from core to skin and by stopping all locomotory activities including feeding, thereby avoiding deterioration of vital organs and physiological processes due to hyperthermia.

Animals↗

Clinical analysis of Fuchs' heterochromic cyclitis.

Fuchs' heterochromic cyclitis (FHC) is an important diagnosis to make. Not only for the patient, because incorrect diagnosis may lead to unnecessary therapy and the failure to detect secondary glaucoma, but also for the comparison of studies on the etiology of FHC, which is still unknown. No clinical criteria for establishing the diagnosis of FHC have been internationally accepted yet. By means of clinical analyses of FHC patients in different parts of the world, predominant clinical features may be distinguished and combined to form (internationally accepted) diagnostic criteria. We report a clinical analysis of 51 FHC patients in the Netherlands. Acute symptoms (severe redness, pain or photophobia) were never (100%) encountered. Characteristic keratic precipitates (88%) and/or minimal aqueous cells and flare (60%) and/or vitreous opacities (84%) were major signs, indicating a chronic inflammatory activity, in which no synechiae (100%) were present. Heterochromia (82%) was not a constant sign, but iris stromal atrophy, which causes the heterochromia, was always present (100%). Cataract was present in 82% as a result of the chronic iridocyclitis. Secondary glaucoma was present in 22%. Based on the predominant clinical findings obtained from this analysis of FHC patients, and on data in the literature, we propose clinical diagnostic criteria for FHC. Future studies, also including other uveitis groups, are necessary to confirm these diagnostic criteria.

Adolescent↗

Accelerations due to impact at heel strike using below-knee prosthesis.

The acceleration in the sagittal plane of the prosthetic tube at heel strike in normal walking was measured in five healthy amputees with their definitive below-knee prosthesis, every subject using six different prosthetic feet, wearing sport shoes as well as leather shoes. The experiments were carried out in the rehabilitation centre "Het Roessingh", Enschede, The Netherlands. Maximum accelerations were extracted from the acceleration-time-signal. Mean acceleration maxima of all subjects were calculated for each foot-shoe combination to eliminate the individual influence of the subjects. In the axial direction the maximal accelerations demonstrate a clear difference among the prosthetic feet and the shoes, while in dorsoventral (tangential) direction the inter-individual variation in the acceleration extremes dominates the difference between the types of footwear. In comparison with non-amputees the magnitude of the maximal axial acceleration at heel strike does not differ significantly.

Amputees↗

Reduction by acetylsalicylic acid of paracetamol-induced hepatic glutathione depletion in rats treated with 4,4'-dichlorobiphenyl, phenobarbitone and pregnenolone-16-alpha-carbonitrile.

The role of enzyme induction in the reduction by acetylsalicylic acid (ASA) of paracetamol-induced hepatic glutathione (GSH) depletion has been studied in rats. Administration of an overdose of paracetamol to control rats resulted in an appreciable decrease of GSH concentration. Pretreatment with the enzyme inducers phenobarbitone, 3-methylcholanthrene (3-MC), pregnenolone-16-alpha-carbonitrile (PCN) and 4,4'-dichlorobiphenyl (4,4'-DCB) significantly potentiated the paracetamol-induced depletion of GSH. Simultaneous administration of an equimolar dose of ASA resulted in a reduction of the paracetamol-induced depletion of GSH in all instances except for those rats that were not pretreated and those given 3-MC. Benorylate, the ASA ester of paracetamol, depressed rat liver GSH to levels comparable to those produced by the combination of paracetamol and ASA. ASA itself caused only minor changes in liver GSH concentrations. The results demonstrate that ASA causes a diminution of paracetamol-induced GSH depletion in rats with phenobarbitone type of enzyme induction. Inhibition of the formation of the reactive metabolite of paracetamol or reduction of the absorption rate of paracetamol seem to be unlikely as mechanisms underlying the ASA-induced effect. An ASA-mediated effect via changes of the hepatic thiol status is proposed.

Acetaminophen↗

Spinal cord transections in fetal rats. Open intrauterine surgery with low mortality.

Open myelotomies were performed in rat fetuses in stages E15-E19 with a microsurgical technique. To prevent oligohydramnios, considered to be one of the main causes of death associated with fetal surgery, amniotic fluid loss was reduced as much as possible. With this technique a reduction of the mortality rate to 38% was reached in 75 consecutive fetuses.

Animals↗

IL-4 is an essential factor for the IgE synthesis induced in vitro by human T cell clones and their supernatants.

The property of 109 CD4+ T cell clones (TCC) to induce IgE synthesis in vitro in human B cells was compared with their ability to produce IL-2, IL-4, and IFN-gamma in their supernatants (SUP) after 24-h stimulation with PHA. A significant positive correlation was found between the property of TCC to induce or enhance spontaneous IgE synthesis and their ability to release IL-4. In contrast, there was an inverse relationship between the IgE helper activity of TCC and their ability to release IFN-gamma, whereas no statistical correlation between the property to induce IgE synthesis and to produce IL-2 was observed. The ability of PHA-SUP from 71 CD4+ TCC to induce IgE synthesis in B cells was also investigated. Twenty-nine SUP (all derived from TCC active on IgE synthesis) induced production of substantial amounts of IgE in target B cells. There was a correlation between the amount of IgE synthesized by B cells in response to these SUP and their IL-4 content. An even higher correlation was found between the IgE synthesis induced by these SUP and the ratio between the amount of IL-4 and IFN-gamma present in the same SUP. Like IL-4-containing SUP, rIL-4 also showed the ability to induce IgE production in B cells from both atopic and nonatopic donors. The addition to B cell cultures of anti-IL-4 antibody virtually abolished not only the IgE synthesis induced by rIL-4, but also that stimulated by TCC and their SUP. In contrast, the IgG synthesis induced by TCC SUP was not or only slightly inhibited by the anti-IL-4 antibody. These data indicate that IL-4 is an essential mediator for the IgE synthesis induced in vitro by human TCC and their SUP in the absence of a polyclonal activator, whereas IFN-gamma seems to exert a negative regulatory effect on the production of IgE.

Adult↗

Response of LFA-1-deficient B cells to interleukin 4 (BSF-1) and low molecular weight B cell growth factor (BCGFlow).

T cell-depleted B cells from a patient with LFA-1 deficiency were tested in costimulation assays for responsiveness to recombinant human IL4 (BSF-1) and purified low molecular weight B cell growth factor (BCGFlow). In both cases the response of LFA-1-deficient B cells was comparable with normal controls. Monoclonal antibodies to LFA-1 alpha (CD11a) and beta (CD18) chains were unable to mimic the action of IL4 on normal B cells in costimulation assays with anti-IgM, and did not inhibit normal B cell proliferation in response to IL4 and anti-IgM. Epstein-Barr virus-transformed lymphoblastoid B cell lines (LCL) from normal and LFA-1-deficient donors both responded in proliferation assays to BCGFlow but not IL4. Similarly, both normal and LFA-1-deficient LCL increased IgM secretion in response to BCDF, BCGFlow and, interestingly, IL4. The normal LCL also increased IgG secretion in response to these factors, but no IgG was detected in supernatants from the LFA-1-deficient LCL. These results show that LFA-1 expression is not essential for B cell responses to B cell growth and differentiation factors.

Antibodies, Monoclonal↗

Induction of interleukin-4-dependent IgE synthesis and interleukin-5-dependent eosinophil differentiation by supernatants of a human helper T-cell clone.

The human alloreactive T-cell clone A1 produces interleukin (IL)-4, IL-5, and granulocyte macrophage-colony stimulating factor (GM-CSF), but not IL-2 or interferon-gamma (IFN-gamma), as assessed by probing for mRNA transcripts, immunoassays, or bioassays. Supernatants from clone A1 induced IgE synthesis by normal human peripheral blood mononuclear cells. IL-4 was shown to be necessary and sufficient for the induction of IgE by clone A1 supernatants. In contrast, IgE induction by clone A1 supernatants and recombinant (r) IL-4 was inhibited by IFN-gamma. This suggests that the absence of IFN-gamma from the IL-4-containing A1 supernatants was important for their IgE-inducing ability. Supernatants from clone A1 could also specifically induce the growth of cord blood cell progenitors and their differentiation into eosinophils but not into basophils. rIL-5, but not rIL-4 or rGM-CSF, also induced eosinophil maturation. These data suggest that IL-5 secreted by clone A1 was responsible for its ability to induce eosinophil differentiation. The implications of the concomitant production of IL-4 and IL-5 by a single T-cell clone are discussed.

Cell Differentiation↗

The effect of fibrin sealant on mouse embryos.

It is postulated that ovarian hyperstimulation prior to embryo transfer results in changes in the endometrium which lead to poor adhesive properties of the endometrium. Based on the properties of fibrin sealant which is used in human operative medicine, it is believed that adhesion of embryos to the endometrium during embryo transfer may be encouraged by the addition of fibrin sealant. The purpose of this study was to assess the effects of the addition of fibrin sealant to a mouse embryo/Ham's F-10 culture medium mixture. There was no statistical difference in the number of blastocysts developing from 138 embryos in standard medium compared with 139 cultured with the addition of fibrin sealant. It is concluded that fibrin sealant is not embryotoxic, and thus following further experimentation its eventual utilization in human in vitro fertilization/embryo transfer programs appears promising.

Animals↗

Coordinate regulation of immune and inflammatory responses by T cell-derived lymphokines.

In response to antigenic stimulation, helper T cells secrete a set of protein mediators called lymphokines that regulate proliferation, differentiation, and maturation of lymphocytes and hemopoietic cells. Because all known lymphokines are composed of a single polypeptide chain, their coding sequences can be isolated by functional expression in appropriate host cells. Based on this expression cloning protocol, a number of T cell lymphokine genes have been isolated, their primary structure has been determined, and biological properties of their recombinant products have been examined. These studies revealed the existence of a regulatory network between lymphoid cells and hemopoietic cells mediated by the actions of multiple pleiotropic lymphokines produced by activated T cells. Because all or a part of this network can be activated in different ways by unique combinations of lymphokines, it is clear that T cells can play a vital role in coordinating the function of different body compartments in the immune and inflammatory responses. The activation of lymphokine genes in T cells by antigen is rapid and temporal. Therefore, an inflammatory response that involves proliferation and maturation of target cells may be restricted to the site of lymphokine production. This inducible hemopoiesis appears to be differentially regulated from the steady state or constitutive hemopoiesis that occurs in the bone marrow microenvironment in the absence of immunological stimuli.

Animals↗

Semi-quinone formation from the catechol and ortho-quinone metabolites of the antitumor agent VP-16-213.

The catechol metabolite of the antitumor agent VP-16-213 and the ortho-quinone of VP-16-213--a secondary metabolite formed from the catechol--easily undergo auto-oxidation into a free radical at pH greater than or equal to 7.4. By elevation of the pH from 7.4 to 10, an increase in the production of the free radical was observed, which was accompanied by the formation of products with higher hydrophylicity than the catechol and ortho-quinone, as found by HPLC-analysis. The hyperfine structure of the free radical indicates that it is the semi-quinone radical of VP-16-213. At pH 12.5 a secondary radical is formed from the catechol and the ortho-quinone of VP-16-213 besides the semi-quinone radical. One-electron oxidation of the catechol with horseradish peroxidase/hydrogen peroxide resulted in the formation of the same radical as observed under alkaline conditions and subsequent oxidation to the ortho-quinone. If the ortho-quinone was incubated with NADPH cytochrome P-450 reductase, a free radical was detected by spin-trapping with POBN, but not without spin-trapping. Studies on inactivation of phi X174 DNA by the system ortho-quinone of VP-16-213/NADPH cytochrome P-450 reductase suggest that the semi-quinone radical may play a role in the process of inactivation of DNA.

Bacteriophage phi X 174↗

MPP+-induced efflux of dopamine and lactate from rat striatum have similar time courses as shown by in vivo brain dialysis.

Perfusion of rat striatum with 10 mM 1-methyl-4-phenylpyridinium (MPP+) during 1 min caused a rapid reversible increase in dopamine (DA) efflux (maximal after 4 min) that was similar to the effects of 1 or 15 min 10 mM amphetamine. A massive, prolonged, and irreversible release of DA occurred after 15 min 10 mM MPP+, showing a biphasic trend: the rapid amphetamine-like increase was followed by a slower and larger DA efflux, reaching its maximum after 25 min. One minute perfusions with 1-100 mM MPP+ caused a gradual increase in the overflow of striatal lactate, reaching a maximum effect after 20-30 min. The similarity between the time courses of the MPP+-induced efflux of DA and lactate suggests that both effects are probably consequences of inhibition of aerobic glycolysis by MPP+. A comparison with the courses of DA and lactate efflux after death of control rats showed a delay of several minutes before the toxic effects of MPP+ become apparent. These in vivo data are consistent with the hypothesis that MPP+ accumulates and then kills dopaminergic cells, possibly by the irreversible inhibition of mitochondrial respiration.

1-Methyl-4-phenylpyridinium↗