Incompatibility of contrast agents with intravascular medications. Work in progress

In vitro and in vivo precipitation of iodinated contrast agents when ioxaglate and papaverine are given together has been reported. To verify these reports and to investigate other medications not previously tested, the authors analyzed mixtures of contrast agents and medications in vitro with a light spectrophotometer and observed them for visible precipitates for up to 120 minutes. Previously reported incompatibilities between ionic or low-osmolality contrast media and medications were verified, and several new incompatibilities were discovered. No incompatibilities were found when the drugs tested were mixed with the new nonionic contrast media.     

Chlamydial etiology of acute lower respiratory tract infections in children in the Sudan

The role of Chlamydia pneumoniae in 110 Sudanese children with signs of acute lower respiratory tract infections (ALRI) was investigated. Four (3.6%) had evidence of C. pneumoniae infection, of whom 3 were culture-positive, while 1 had an antibody response suggesting a recent infection. IgG antibodies at a titer of ≥1:32 to C. pneumoniae, Chlamydia psittaci and Chlamydia trachomatis were detected in 27 (24.5%), 27 (24.5%) and 7 (6.4%) of the 110 ALRI cases, respectively. C. pneumoniae, C. trachomatis or C. psittaci were not detected in nasopharyngeal secretions from any of 110 patients when fluorescence-labeled specific monoclonal antibodies were used. In a seroepidemiological survey, 318 healthy Sudanese persons aged between 1 month and 67 years were studied for C. pneumoniae antibodies.     

Sweet's syndrome—therapy with cyclosporin

We report the case of a 39-year-old female patient suffering from Sweet's syndrome after an upper respiratory tract infection. Cyclosporin A at a dose of 10 mg/kg per day was given as initial treatment. Skin lesions and general malaise resolved within 9 days. The cyclosporin dose was decreased within 21 days, without recurrence of the eruption. Cyclosporin is a potent inhibitor of T lymphocytes, but affects granulocyte and monocyte functions as well. Success of treatment in our case shows that cyclosporin represents an alternative to steroid treatment in patients with Sweet's syndrome.     

The persistence of interleukin-6 is regulated by a blood buffer system derived from dendritic cells

1. Download : Download high-res image (129KB)
2. Download : Download full-size image

     

Time-resolved particle image velocimetry and laser doppler anemometry study of the turbulent flow field of bileaflet mechanical mitral prostheses

Dynamic particle image velocimetry (PIV) was applied to the study of the flow field associated with prosthetic heart valves. The results were compared with those of laser Doppler anemometry (LDA). Anatomically and antianatomically oriented Jyros (JR) and St. Jude Medical (SJM) valves were compared in the mitral position to study the effects of valve design on the downstream flow field. The experimental program used a dynamic PIV system utilizing high-speed, high-resolution video to map the true time-resolved velocity field inside the simulated ventricle. This system was complemented by a study using the more traditional LDA system for comparison. Based on the experimental data, the following general conclusions can be made. High-resolution dynamic PIV can capture true chronological changes in the velocity and turbulence fields. It also produces very detailed velocity and turbulence information comparable to the LDA results. In the vertical measuring plane that passes both the center of the aortic and mitral valves (A-A section), the two valves (the SJM and the JR) show distinct circulatory flow patterns when the valve is installed in the antianatomical orientation. Small differences in valve design can generate noticeable differences, particularly during the accelerating flow phase. The SJM valve maintains a relatively high velocity through the central orifice; the curved leaflets of the JR valve generate higher velocities with a divergent flow during the accelerating and peak flow phases. In the velocity field directly below the mitral valve and normal to the previous measuring plane (B-B section), where characteristic differences in valve design will be visible, symmetrical twin circulations were observed because of the divergent nature of the flow generated by the two inclined half-disks installed in the antianatomical orientation. The SJM valve, with a central downward flow near the valve, is contrasted with the JR valve, which has a peripheral downward circulation with higher, turbulent stresses.     

Induction by sphingomyelinase of shiga toxin receptor and shiga toxin 2 sensitivity in human microvascular endothelial cells

Shiga toxin-producing enterohemorrhagic Escherichia coli is the major cause of acute renal failure in young children. The interaction of Shiga toxins 1 and 2 (Stx1 and Stx2) with endothelial cells is an important step in the renal coagulation and thrombosis observed in hemolytic uremic syndrome. Previous studies have shown that bacterial lipopolysaccharide and host cytokines slowly sensitize endothelial cells to Shiga toxins. In the present study, bacterial neutral sphingomyelinase (SMase) rapidly (1 h) sensitized human dermal microvascular endothelial cells (HDMEC) to the cytotoxic action of Stx2. Exposure of endothelial cells to neutral SMase (0.067 U/ml) caused a rapid increase of intracellular ceramide that persisted for hours. Closely following the change in ceramide level was an increase in the expression of globotriaosylceramide (Gb3), the receptor for Stx2. A rapid increase was also observed in the mRNA for ceramide:glucosyltransferase (CGT), the first of three glycosyltransferase enzymes of the Gb3 biosynthetic pathway. The product of CGT (glucosylceramide) was also increased. In contrast, mRNA for the third enzyme of the pathway, Gb3 synthase, was constitutively produced and was not influenced by SMase treatment of HDMEC. These results describe a rapid response mechanism by which extracellular neutral SMase derived from either bacteria or eukaryotic cells may signal endothelial cells to become sensitive to Shiga toxins.