Cardiogenic shock: A look at acute functional mitral incompetence.

A 44-year-old man presented with cardiogenic shock secondary to acute functional mitral incompetence as well as septic shock related to pneumonia. The patient deteriorated haemodynamically despite adequate medical therapy. An echocardiogram revealed a massive mitral incompetence and an ejection fraction of 32%. An intra-aortic balloon pump was placed and the patient improved dramatically. On day 6 after admission the echocardiogram was repeated, revealing a mild mitral incompetence and an ejection fraction of 58%.

Direct and indirect cellular effects of aspartame on the brain.

The use of the artificial sweetener, aspartame, has long been contemplated and studied by various researchers, and people are concerned about its negative effects. Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and methanol (10%). Phenylalanine plays an important role in neurotransmitter regulation, whereas aspartic acid is also thought to play a role as an excitatory neurotransmitter in the central nervous system. Glutamate, asparagines and glutamine are formed from their precursor, aspartic acid. Methanol, which forms 10% of the broken down product, is converted in the body to formate, which can either be excreted or can give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives. Previously, it has been reported that consumption of aspartame could cause neurological and behavioural disturbances in sensitive individuals. Headaches, insomnia and seizures are also some of the neurological effects that have been encountered, and these may be accredited to changes in regional brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine. The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning.

Radiation dose estimates of 186Re-hydroxyethylidene diphosphonate for palliation of metastatic osseous lesions: an animal model study.

A common complication in patients with breast or prostate cancer is bone metastases causing pain. New radionuclide therapy methods have recently been proposed for palliation, including 186Re-hydroxyethylidene diphosphonate (186Re-HEDP). This paper reports on the local development of 186Re-HEDP and the biodistribution studied in animals for eventual use in patients. Adult dose was computed assuming a 70 kg standard man. The 186Re was labelled to HEDP using standard techniques. The biodistribution in five Chacma baboons (Papio ursinus) was studied. Doses ranging from 39.4 to 44.9 MBq kg(-1) (mean 43.6 +/- 2.8 MBq kg[-1]) were administered, corresponding to an adult human dose of 2960 MBq (80 mCi). Whole-body images of the animals were obtained with a dual-headed scintillation camera on an hourly basis for 6 h post-injection and then daily for 3 days. The bone, soft tissue, kidneys and urinary bladder were considered source organs and data from these organs were used in a compartmental model to obtain the mean residence times of the radionuclide in the different source organs. Radiation dose estimates for 186Re-HEDP were subsequently obtained with the MIRDOSE 3 program. The estimated absorbed radiation doses to some of the organs (expressed in mGy MBq[-l]) were as follows: bone surface 1.69; kidneys 0.09; liver 0.04; ovaries 0.04; red marrow 0.75; total body 0.12; urinary bladder wall 0.43. 186Re-HEDP yielded an effective dose of 0.17 mSv MBq(-1). The radiation dose delivered to the bone marrow in this study did not cause any detrimental effect to the baboons, indicating that locally produced 186Re-HEDP is suitable for clinical use.

A Monte Carlo evaluation of the channel ratio scatter correction method.

Several methods exist to eliminate the contribution of scattered photons during imaging. One of these, the channel ratio (CR) scatter correction technique, uses the change in the ratio of counts from two symmetrical adjacent energy windows straddling the energy photopeak. The accuracy of the results depends upon the assumption that the ratio of the scatter components in the two windows (H value) is constant and is independent of the relative size of the scatter contribution. In this study a Monte Carlo simulation was used to investigate the behaviour of the scatter component for different source sizes at different depths. Four disc sources containing a 99Tcm solution were simulated at different depths as imaged with a scintillation camera. Two 10% energy windows with 5% offsets to either side of the 140 keV photopeak of 99Tcm were used. The ratio of the scattered counts in the lower energy window to the scattered counts in the upper window (true H value) was determined from the simulation for each source at every depth. Since it is impossible to measure the true H value at different organ depths during a clinical study, the use of an average H value was considered. Scatter correction was applied to the images simulated at the various depths in water. The geometric mean was calculated and attenuation correction performed assuming mono-exponential attenuation. For quantitation purposes the corrected counts were expressed in terms of a references source. The choice of the reference source yielding the best quantitative results was also investigated. Results of this Monte Carlo simulation study show that although the true H value depends on both source size and depth of the source in the scattering medium, the CR scatter correction technique can be applied successfully when an average H value is used.

Reference values for red cell survival times.

The first purpose of this investigation was to investigate in 35 young normal male subjects the use of the Dornhorst function and the weighted-mean method to calculate reference values for mean red cell survival time with and without correction for elution of 51Cr. We compared survival times calculated with the Dornhorst and weighted-mean methods with survival time estimated with linear or exponential models. Two methods to correct for elution of 51Cr from red cells were investigated. For the first method, correction factors were generated using the Dornhorst function fitted to mean survival curves obtained from the normal subjects. In the second method, the new Dornhorst rate constant method, the survival time, corrected for elution of 51Cr, was directly calculated from the experimental survival curve without applying correction factors. Correction for elution using the Dornhorst rate constant method was not successful and resulted in nonphysiologic values. The 95% confidence range of red cell survival time for reference subjects without correction for 51Cr elution was 37-74 days for the weighted-mean method and 37 to 73 days for the Dornhorst method. The 95% confidence range for normal subjects when the survival curves were corrected for elution was 47-179 days for the Dornhorst method and 58-161 days for the weighted-mean method. The poor results obtained with the Dornhorst rate constant method and the large 95% confidence range were due to the rapid and large variation in elution rate of 51Cr from red cells.