Identification of antiarrhythmic drugs and their metabolites in urine

Identification of the antiarrhythmic drugs ajmaline, aprindine, diltiazem, disopyramide, flecainide, gallopamil, lidocaine, lorcainide, mexiletine, phenytoin, prajmaline, propafenone, quinidine, sparteine, tocainide and verapamil and their metabolites in urine is described. After acid hydrolysis of the conjugates, extraction and acetylation, the urine samples were analysed by computerized gas chromatography-mass spectrometry. Using ion chromatography with the selective ions m/z 58, 72, 84, 86, 136, 224, 266, and 426, the possible presence of antiarrhythmic drugs and/or their metabolites was indicated. The identity of positive signals in the reconstructed ion chromatograms was confirmed by a visual or computerized comparison of the stored full mass spectra with the reference spectra. The ion chromatograms, reference mass spectra and gas chromatographic retention indices (OV-101) are documented. The method presented is integrated in a general screening procedure (general unknown analysis) for several groups of drugs.     

Microscopic haematuria as a relative contraindication for tranexamic acid

Tranexamic acid has been advocated for patients with severe bleeding tendency due to thrombocytopenia not responding to platelet transfusions. Macroscopic haematuria is a well-known contraindication for its use in such patients. We present three clinical cases with microscopic haematuria, in whom tranexamic acid caused problems of clot formation in the urinary tract, indicating that microscopic haematuria should also be considered as a contraindication for tranexamic acid.     

Large striatocapsular infarcts: Clinical features and risk factors

We defined large striatocapsular infarcts as subcortical softenings of more than 20 mm in diameter involving the territories of the lateral and medial groups of lenticulostriate arteries. The aim of this study of 56 patients was to compare the clinical features and risk factors of these infarcts with those of cortical and lacunar infarcts. On the whole, our data suggest that both the clinical features and risk factors of large striatocapsular infarcts are similar to those of cortical infarcts, but significantly different from those of lacunar infarcts. The clinical manifestations of large striatocapsular infarcts with a maximum diameter of less than 50 mm may sometimes resemble those of lacunar infarcts because neuropsychological disorders are less frequent; however, our study indicates that, even in these cases, cardioembolic sources and artery-to-arteiy embolism are significantly more frequent in large striatocapsular than in lacunar infarcts, thus suggesting a different pathogenesis.     

k-t2 BLAST: exploiting spatiotemporal structure in simultaneously cardiac and respiratory time-resolved volumetric imaging.

Multidimensional imaging resolving both the cardiac and respiratory cycles simultaneously has the potential to describe important physiological interdependences between the heart and pulmonary processes. A fully five-dimensional acquisition with three spatial and two temporal dimensions is hampered, however, by the long acquisition time and low spatial resolution. A technique is proposed to reduce the scan time substantially by extending the k-t BLAST framework to two temporal dimensions. By sampling the k-t space sparsely in a lattice grid, the signal in the transform domain, x-f space, can be densely packed, exploiting the fact that large regions in the field of view have low temporal bandwidth. A volumetric online prospective triggering approach with full cardiac and respiratory cycle coverage was implemented. Retrospective temporal interpolation was used to refine the timing estimates for the center of k-space, which is sampled for all cardiac and respiratory time frames. This resulted in reduced reconstruction error compared with conventional k-t BLAST reconstruction. The k-t(2) BLAST technique was evaluated by decimating a fully sampled five-dimensional data set, and feasibility was further demonstrated by performing sparsely sampled acquisitions. Compared to the fully sampled data, a fourfold improvement in spatial resolution was accomplished in approximately half the scan time.     

Attachment loss and serum antibody levels against autologous and reference strains of Actinobacillus actinomycetemcomitans in untreated localized juvenile periodontitis patients

Abstract Immunological data have been suggested to be a potential tool in the diagnosis, classification and monitoring of periodontal diseases. However, the role of circulating antibodies in periodontal patients is poorly understood. Patients suffering from localized juvenile periodontitis (LJP) are often reported to show high titers of serum IgG antibodies against Aetinobaeillus actinomycetemcomitans (A. actinomycetemcotnitans), but several affected patients do not. Most studies use well-known reference strains of the bacterium for testing against the patients' sera. The aim of the present investigation was to study the relationship between serum IgG antibody levels to autologous A. actinomycetemcomitans strains and clinical attachment loss (CAL). In addition, we wanted to assess the patients’serum titers against 4 well-known reference strains of the bacterium as well as their general potential immunoglobulin response. Intravenous blood samples were taken from 23 LJP patients and 10 healthy individuals, and autologous A. actinomycetemcomitans strains were cultured from 18 of the L.JP patients. CAL was measured at 4 different sites around ail present teeth and assessed as a % of teeth with at least 1 site moderately ≥2<5 mm) or severely (≥5 mm) involved. An enzyme-linked immunosorbent assay (ELISA) was performed to evaluate the serum titers of IgG antibodies to A. actinomycetemcomitans antigens. No significant correlation was found between serum IgG antibody titers to autologous strains and CAL. However, there was a trend that low responders had more moderately affected teeth than had high responders and patients with undetectable A. actinomycetemcomitans levels, which is in agreement with a hypothetically protective role of the antibodies. The total counts of immunoglobulin assessed in all participants showed that the predominant class was IgG and the reference group displayed significantly less (p<0.05) IgG and IgG1 counts than the LJP patients. Both the reaction pattern against reference and autologous strains varied widely. We conclude that the specific antibody response against A. actinomycetemcomitans shows a weak correlation to clinical attachment levels in LJP patients.