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Biomedical subjects

M R Visser

Publications and source records attributed to M R Visser.

68 records · Page 4Linked to original sources
PubMed1991

Comparative in vitro antibacterial activity of sparfloxacin (AT-4140; RP 64206), a new quinolone.

The in vitro activity of sparfloxacin (AT-4140; RP 64206), a new fluoroquinolone, was compared with those of 10 other agents against 1,222 clinical isolates. Sparfloxacin and ciprofloxacin were the most active quinolones against members of the family Enterobacteriaceae and nonfermenting gram-negative bacilli; sparfloxacin had superior activity against gram-positive cocci in comparison with the activities of ciprofloxacin and the other quinolones tested (norfloxacin, lomefloxacin, and pefloxacin). Among the inhibited strains, several were resistant to the tested beta-lactam antibiotics or to aminoglycosides. The activity of sparfloxacin was not influenced by the medium that was used; lowering of the pH to 5 had a marked effect on the MICs for two strains each of Enterobacter cloacae and Pseudomonas aeruginosa and one strain each of Escherichia coli and Staphylococcus aureus; the MBC of sparfloxacin was within 1 to 2 dilution steps of the MIC for the strains that were tested.

4-Quinolones↗
PubMed1989

Comparative in vitro antibacterial activity of the new carbapenem meropenem (SM-7338).

The in vitro antimicrobial activity of the new carbapenem meropenem (SM-7338) was determined by an agar dilution method in comparison with imipenem, ticarcillin/calvulanic acid, ceftazidime and the fourth-generation cephalosporin cefepime (BMY 28142). Meropenem showed superior activity against Enterobacteriaceae (MIC90 less than or equal to 0.06 mg/l) and against non-fermentative gram-negative rods, with the exception of Xanthomonas maltophilia. Meropenem had excellent activity against beta-lactamase-producing Haemophilus influenzae and Neisseria gonorrhoeae, and against the Bacteroides fragilis group. Imipenem was slightly more active then meropenem against gram-positive cocci especially Enterococcus faecalis.

Anti-Bacterial Agents↗
PubMed1989

Herpes simplex virus inhibits endothelial cell attachment and migration to extracellular matrix proteins.

Herpes simplex virus (HSV) infection may be involved in various endothelial-injury syndromes, including vasculitis and atherosclerosis. In a previous study, it was reported that HSV-infected human umbilical endothelial cells are more vulnerable to detachment mediated by granulocyte-secreted proteases. To elucidate the molecular basis of this observation, the authors examined the interaction of infected endothelial cells with the purified basement membrane proteins, fibronectin, laminin, and type IV collagen. HSV-infected endothelial cells exhibited defects in their ability to adhere, spread, and migrate on all three matrix components. This defective adhesion could be partially overcome by increasing concentrations of fibronectin; in contrast, no abrogation of deficient binding occurs with increased levels of laminin or collagen type IV. This suggests that endothelial cells may use different surface constituents for binding to the three proteins and use multiple "receptors" for adhesion to the fibronectin molecule--"receptors" that are variably affected by HSV infection. The authors investigated this supposition by assaying adhesion of normal and infected endothelial cells to two non-overlapping cell-adhesion promoting fragments of fibronectin: 1) a 75 kd motility-promoting fragment which contains the arginyl-glycyl-aspartylserine (RGDS) adhesion sequence, and 2) a 33 kd carboxyl-terminal heparin binding fragment, which promotes cell adhesion by an RGDS-independent mechanism. Normal endothelial cells adhered and spread on both purified fragments. In contrast, while infected endothelial cells could adhere, albeit rather poorly, to high coating concentrations of the 75 kd fragment, these cells did not bind to the 33 kd heparin binding fragment of fibronectin at all. These results support the concept that endothelial cells adhere to multiple domains of fibronectin, and that HSV infection preferentially abrogates binding to the heparin-binding domain, while leaving relatively intact receptors for the RGDS-containing domain. In support, soluble RGDS significantly blocked fibronectin adhesion of infected, but not control, endothelial cells. It is concluded that HSV infection inhibits the interaction of endothelial cells with basement membrane proteins and weakens their tethering to substratum. This tethering is inadequate for proper cell spreading or movement to occur and may result in both excessive endothelial lift-off and impaired vascular repair in HSV infections.

Cell Adhesion↗
PubMed1989

Granulocyte-mediated injury to herpes simplex virus-infected human endothelium.

Some endothelial-injury syndromes, including atherosclerosis, may involve herpes simplex virus (HSV) infection. Examining the mechanism of injury, we found adherence of unstimulated granulocytes to HSV infected endothelium to be twice that to uninfected endothelium (34.8 +/- 1.1 versus 18.8 +/- 0.5%; mean +/- SEM; p less than 0.001) which further increased in the presence of anti-HSV antibodies. Enhanced adhesion was accompanied by excessive granulocyte-mediated lysis of 51Cr-labeled, HSV-infected endothelium (16.4 +/- 0.9%, HSV-infected versus 0.9 +/- 4.5% for uninfected endothelium; p less than 0.01). HSV infection also increased granulocyte-mediated endothelial cell detachment from its substratum (14.7 +/- 1.7% versus 3.3 +/- 0.3% for uninfected endothelium; p less than 0.001), which further increased (p less than 0.01) in the presence of immune complexes (IgG-sensitized erythrocytes). This suggests that neo-Fc receptors of infected endothelium bind IgG-coated particles, which, in turn, attract and stimulate granulocytes. In support, granulocyte-mediated detachment was not enhanced by immune complexes if endothelium was infected with a mutant HSV strain (E3/3) that does not produce glycoprotein E, the viral glycoprotein having Fc-receptor activity. Exaggerated endothelial detachment correlated with poor binding of infected endothelial cells to the substratum matrix protein, fibronectin. Resuspended, virus-infected endothelial cells bound significantly less well to tissue-culture wells coated with both low (p less than 0.001) and high (p less than 0.05) concentrations of fibronectin as compared with uninfected endothelial cells, a dichotomy further worsened in the presence of granulocyte-released elastase. We conclude that HSV-infected human endothelium is vulnerable to granulocyte-mediated injury by opposing alterations in its adhesive properties: its increased binding of granulocytes and its weakened tethering to matrix fibronectin, particularly when exposed to secreted granulocyte proteases, such as elastase.

Cell Adhesion↗
PubMed1988

Enhanced thrombin generation and platelet binding on herpes simplex virus-infected endothelium.

Atherosclerotic lesions have been reported to contain herpes simplex virus 1 (HSV-1) genomic material. This, and other previous evidence, suggests that latent viral infection may be an atherogenic trigger. Moreover, active HSV-1 lesions manifest marked fibrin deposition in microvessels. In this report we show that very early infection of human endothelial cells with HSV-1 appears to alter surface conformation as detected by merocyanine 540 staining. Concomitantly, the efficiency of prothrombinase complex assembly increases, resulting in a 2- to 3-fold accelerated rate of thrombin generation on the cell surface. Increased thrombin generation is probably doubly procoagulant, since we also demonstrate that thrombin-induced platelet accumulation on HSV-infected endothelium (50.7 +/- 9.3%) is increased compared to uninfected endothelium (9.5 +/- 2.1%; P less than 0.002). Associated with HSV infection, prostacyclin secretion in response to thrombin is diminished by a factor of 20, probably explaining the enhanced platelet attachment. We conclude that HSV infection shifts endothelial cell properties from anticoagulant to procoagulant, both by promoting prothrombinase complex formation and function and by increasing platelet binding, well before cell disruption takes place. Virus-induced changes in the endothelial plasma membrane and diminished prostacyclin secretion are suggested as the pathways for this pathophysiologic mechanism, which may be germane to atherosclerotic thrombosis as well as HSV-mediated tissue necrosis.

Arteriosclerosis↗
PubMed1988

Measurement of intracellular calcium concentration in intact monolayers of human endothelial cells.

Intracellular calcium ([Ca++]i) plays an important role in signal transduction and cell activation. The measurement of [Ca++]i in intact monolayers of human umbilical vein endothelial cells with the fluorescent calcium-sensitive probe fura 2 has been evaluated. Monolayers provide a more physiologic cell preparation than suspensions and allow a greater variety of experimental manipulation. Basal [Ca++]i was 117 +/- 5 nmol/L, with a range from 40 to 280 nmol/L that was not affected by cell age (days of primary culture) or degree of confluence. Thrombin in concentrations of 0.005 to 5 NIH units/ml produced a dose-dependent increase in [Ca++]i up to a maximum of 1500 +/- 147 nmol/L; this increase was shown to depend in part on the concentration of extracellular calcium. The presence of antithrombin III at physiologic concentrations abolished responses to 0.5 NIH units/ml thrombin but had no effect on 5 NIH units/ml. The potential of this technique was demonstrated further by our ability to examine [Ca++]i responses in endothelial cells following infection with herpes simplex virus type 1, a virus implicated in vascular injury. After 18 hours' infection, the response to both thrombin and histamine was dramatically reduced despite a normal resting [Ca++]i. It is concluded that this method may be useful for detecting early and subtle changes in endothelial cell function under a variety of physiologic and pathologic conditions.

Antithrombins↗
PubMed1987

Potentiated adherence of sickle erythrocytes to endothelium infected by virus.

Systemic viral infection is a known precipitant of vasocclusive crisis in sickle patients, but the mechanism underlying this clinical observation is unknown. In the present studies, human umbilical vein endothelial cells were infected with Herpes simplex virus type 1 (HSV) to model systemic viral disease. The already abnormal adherence of sickle erythrocytes to control endothelium is enhanced 1.8 +/- 0.4-fold to HSV-infected endothelium (P less than 0.001). This component of potentiated adherence is eliminated by maneuvers that block Fc receptors, it is prevented by tunicamycin, and it is not seen using a mutant HSV that is unable to express the Fc receptor glycoprotein. Thus, the incremental adherence seen here occurs due to expression of Fc receptor activity on HSV-infected endothelium and the consequent recognition of abnormal amounts of IgG on sickle erythrocytes. We conclude that systemic viral infection potentially can induce a novel mechanism for enhancement of erythrocyte adherence to endothelium and that this may increase the likelihood of vasocclusion during viral infection.

Anemia, Sickle Cell↗
PubMed1986

Measurement of antibody-mediated binding of human polymorphonuclear leukocytes to HSV-1 infected anchorage fibroblasts.

A method for the quantitation of effector cell binding to anchorage fibroblast monolayers infected with HSV-1 is described. Human peripheral blood polymorphonuclear leukocytes (PMN) as effector cells were labeled with chromium-51. Fetal human lung fibroblasts were grown to confluency in microtiter plates, infected with HSV-1 and loaded with anti-HSV antibody. The amount of radiolabeled PMN adhering to the monolayer was determined after appropriate incubation and washings. The effector binding assay was shown to be dependent on specific anti-HSV antibodies, antibody concentration, HSV viral expression, and inoculation time. This assay system is especially useful for the evaluation of effector to target cell conjugate formation when applied to anchorage target cells.

Antibodies, Viral↗
PubMed1986

Cytotoxicity by human adherent cells: oxygen-dependent and -independent cytotoxic reactions by different cell populations.

Human adherent cells, obtained by EDTA reversible adherence to plastic, are potent effectors in cell-mediated cytotoxicity. Spontaneous cytotoxicity in a 2-hr assay against K562 target cells was shown to be largely mediated by contaminating natural killer (NK) cells. Treatment of adherent cells with NK-specific monoclonal antibody anti-Leu-11 plus complement abolished almost completely the spontaneous cytotoxicity. Spontaneous cytotoxicity by adherent cells was also reduced when the phorbol ester PMA was present in the assay. On the other hand, PMA induced a cytotoxic response in NK-cell depleted adherent cells after prolonged 18 hr incubation. The cell population responsible for this dichotomous effect of PMA on adherent cell-mediated cytotoxicity was shown to be monocytes, as revealed by monoclonal antibody treatment. Pure NK cell preparations were not affected by PMA in their cytolytic capacities. Reactive oxygen species are not involved in NK-cell mediated cytotoxicity, while PMA stimulated the monocytes to exert cytolysis and suppressed NK cells by the generation of these highly toxic oxygen products. Hydrogen peroxide especially seemed to be the mediator in this oxygen-dependent monocyte-mediated cytotoxicity and NK-cell suppression.

Catalase↗
PubMedDate not supplied

The Roter Interaction Analysis System (RIAS) in oncological consultations: psychometric properties.

One of the most frequently used systems to analyse doctor-patient communication is the Roter Interaction Analysis System (RIAS). However, it has mostly been applied and evaluated in primary care settings. Two studies are presented in which the psychometric properties of the RIAS are investigated in an oncological setting. In the first study (N = 25) the feasibility, inter-rater reliability and content validity of the RIAS was investigated. In the second study, we evaluated the discriminant validity of the RIAS. Results of the first study showed that coding of tapes was more time consuming than indicated by the Roter manual. The inter-rater reliability proved to be high for both physician communication (0.68-1) and patient communication (0.60-1). The content validity proved to be acceptable: all utterances could be classified. However, coding dilemmas regarding affective communication occurred. The RIAS provided no option to classify communication of a third person present. Some communication categories were never or rarely used. Results of the second study indicate that the RIAS was able to discriminate between communicative behaviors in oncological consultations (N = 60) and three different GP-samples (random-GP sample N = 329, hypertension sample N = 103, gynaecology sample N = 65). To conclude, the psychometric properties of the RIAS are satisfactory in an oncological setting.

Adult↗
PubMedDate not supplied

Cancer patients' coping styles and doctor-patient communication.

Monitoring and blunting styles have become relevant concepts regarding their potential impact on patients' and doctors' behaviors. The present study aimed at investigating the relation between cancer patients' coping styles and doctor-patient communication and global affect. Coping styles were assessed by means of the Threatening Medical Situations Inventory (TMSI). Since a shortened version of the TMSI was used, the validity of this instrument was also evaluated. First, it was examined whether the two factor structure of the original TMSI could be confirmed in our version. Then, the relation between coping style and patients' preferences for information and participation in decision-making was evaluated. Second, the relation between monitoring and blunting and patients' age, sex, education, quality of life and prognosis was investigated. Finally, the relation between patients' coping styles and communicative behaviors and global affect of both patients and physicians during the initial oncological consultation was examined. Patients (N = 123) visited their gynaecologist or medical oncologist for an initial discussion of possible treatment. Patients' coping styles, socio-demographics, preference for information and participation in decision-making, quality of life and prognosis were assessed by postal questionnaire prior to the visit to the outpatient clinic. The consultation was audiotaped and analysed according to Roter's Interaction Analysis System, to identify instrumental and affective communicative behaviors of both patients and physicians. The two factor structure of the TMSI could be confirmed. A monitoring style was related to a preference for detailed information (r = 0.23) and participation in medical decision-making (r = 0.23). A monitoring style was also related to patient question-asking (r = 0.25) and patient dominance (r = 0.23). To conclude, the validity of the shortened TMSI is satisfactory. Also, cancer patients' coping styles are not related to other personal and disease characteristics. Further, a monitoring style seems to have an impact on patients' question-asking and dominance during the oncological consultation.

Adaptation, Psychological↗
PubMedDate not supplied

Occurrence of extended-spectrum betalactamases (ESBL) in Dutch hospitals.

The prevalence of ESBL was determined among isolates of Escherichia coli (n = 571) and Klebsiella spp. (n = 196) collected during a 1-week study period in 8 university and 3 large regional laboratories all over the Netherlands. 18 isolates were positive for at least one of the screening tests used, i.e., VITEK-ESBL, E-test ESBL and MIC ratio of ceftazidime/ceftazidime-clavulanic acid, cefotaxime/cefotaxime-clavulanic acid. In 5 of these 18 putative ESBLs no betalactamase production was detectable. A TEM type was found in three E. coli and two Klebsiella spp. An SHV type was present in five Klebsiella spp. In one E. coli and one Klebsiella pneumoniae both enzymes were present. In one Klebsiella oxytoca neither of the two enzymes was present. Using PCR for both ESBL TEM and ESBL SHV, an SHV ESBL was found in one E. coli and four Klebsiella isolates. The mutations at position 238 and 240 were already described. In one E. coli isolate a TEM ESBL was found with three mutations, at position 21, 164 and 265. These mutations were already described in other ESBLs but not in this combination suggesting a new TEM ESBL. The overall prevalence of ESBL producing E. coli and Klebsiella spp. was less than 1% (6 out of 767).

Anti-Bacterial Agents↗
PubMedDate not supplied

Septicemia due to coagulase-negative staphylococci in a neonatal intensive care unit: clinical and bacteriological features and contaminated parenteral fluids as a source of sepsis.

During the years 1979 to 1981 we experienced an increasing incidence of septicemia due to coagulase-negative staphylococci in the neonatal intensive care unit (NICU). A detailed analysis was performed for the 1981 NICU population. More than 90% of cases occurred in premature infants of low birth weight (less than 2500 g). All septicemic infants were receiving intravenous therapy and total parenteral nutrition (TPN) solutions had been administered to nearly 80% just before or during the septic episode. A case-control study performed for the 1981 NICU population, which included 26 proved cases of coagulase-negative staphylococcal septicemia and 26 matched controls, did not uncover any differences in underlying diseases or modes of treatment between cases and controls. However, the infusion of contaminated TPN fluids was identified as a significant risk factor. Random bacteriological checks of TPN fluids revealed that nearly 20% of these solutions were contaminated, mainly with coagulase-negative staphylococci. The incidence of staphylococcal septicemia in infants who had received contaminated TPN fluids was 10-fold higher than in infants who had received sterile solutions (P less than 0.0005). The majority of coagulase-negative staphylococci isolated from the blood cultures from the NICU were multiply resistant to antibiotics although all isolates were susceptible to cephalothin. Treatment, consisting of removal or replacement of the intravenous devices and the administration of cephalothin and fresh plasma, was universally successful.

Humans↗