Biomedical informatics in the desert--a new and unique program at Arizona State University.

OBJECTIVES: A new academic Biomedical Informatics (BMI) Program in Phoenix, Arizona, embodies a unique organizational structure to draw on the strengths of a computer science and informatics school and the biomedical and clinical strengths of a college of medicine, in an effort to infuse informatics approaches broadly. METHODS: The program reflects a partnership of two state universities that situates the Arizona State University (ASU) Department of BMI on a new downtown Phoenix Biomedical Campus with the University of Arizona (UA) College of Medicine in partnership with ASU (COM-PHX). Plans call for development of faculty and expertise in the four major subdomains of BMI, as well as in various cross-cutting capabilities. RESULTS: Coming into existence in a state that is investing significantly in biomedical science and technology, BMI has already developed Masters and PhD degree programs, is working with COM-PHX to integrate informatics intensively into the education of the medical students, and has been authorized to plan for an undergraduate program in BMI. Reflecting the statewide emphasis on the biomedical and health sector, the growing faculty are engaged in a number of research partnerships and collaborative centers. CONCLUSIONS: As one of the newest academic BMI programs is taking shape in Arizona, it is embarking on a wide-ranging educational program and a broad research agenda that are now in their earliest stages.

Neural network approach for image chromatic adaptation for skin color detection.

The goal of image chromatic adaptation is to remove the effect of illumination and to obtain color data that reflects precisely the physical contents of the scene. We present in this paper an approach to image chromatic adaptation using Neural Networks (NN) with application for detecting--adapting human skin color. The NN is trained on randomly chosen color images containing human subject under various illuminating conditions, thereby enabling the model to dynamically adapt to the changing illumination conditions. The proposed network predicts directly the illuminant estimate in the image so as to adapt to human skin color. The comparison of our method with Gray World, White Patch and NN on White Patch methods for skin color stabilization is presented. The skin regions in the NN stabilized images are successfully detected using a computationally inexpensive thresholding operation. We also present results on detecting skin regions on a data set of test images. The results are promising and suggest a new approach for adapting human skin color using neural networks.

Characteristics of gait of humans with incomplete spinal cord injury.

Epidural spinal cord stimulation has been demonstrated to help the recovery of walking abilities of patients with incomplete spinal cord injury when combined with partial weight bearing therapy. However, no work has been done in studying the dynamics of these signals generated with and without stimulation. We show that the underlying dynamics of such signals is chaotic. We also estimate the correlation dimension of these signals and show the difference in the dynamics of gait with and without stimulation using the kinematic data of right knee and right hip. The correlation dimension thus estimated can be used to evaluate the efficiency of epidural spinal cord stimulation in patients.

Wavelet-based image coding using nonlinear interpolative vector quantization.

We propose a reduced complexity wavelet-based image coding technique. Here, 64-D (for three stages of decomposition) vectors are formed by combining appropriate coefficients from the wavelet subimages, 16-D feature vectors are then extracted from the 64-D vectors on which vector quantization (VQ) is performed. At the decoder, 64-D vectors are reconstructed using a nonlinear interpolative technique. The proposed technique has a reduced complexity and has the potential to provide a superior coding performance when the codebook is generated using the training vectors drawn from similar images.

The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, induces specific transcription by RNA polymerase III in Drosophila Schneider cells.

We have examined the ability of the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), to regulate RNA polymerase III gene expression in Drosophila. Using nuclear run-on assays, we detected a 3-5-fold increase in tRNA synthesis following treatment of Drosophila Schneider S2 cells with TPA, whereas transcription from the actin 5C, fos-, and jun-related antigen promoters was unaffected. This response is rapid and transient, peaking at about a 45-min exposure of the cells to TPA, and dissipating after 60 min. We have reproduced this stimulation in vitro. Extracts prepared from cells treated with TPA show an approximate 10-fold increase in specific transcription using a 5 S RNA and various tRNA gene templates. The nonspecific transcription by RNA polymerase III in these extracts, however, is essentially unchanged. Mixing the extracts derived from uninduced and induced cells suggests that the TPA stimulation observed may be due to the increase of a positive-acting factor. These results are the first to demonstrate that a phorbol ester can induce RNA polymerase III gene expression. The ability to reproduce this activation in vitro will now allow us to assess the role of the transcription components in this regulatory event, and the biochemical consequence of this signaling pathway.

Diagnostic delay after dimenhydrinate use in vomiting children.

OBJECTIVE: To determine whether the use of dimenhydrinate was associated with delay in the diagnosis and management of treatable illnesses or with direct adverse effects in children with vomiting presenting to an emergency department. DESIGN: Questionnaire survey and review of drug reaction and telephone inquiry records. SETTING: The emergency department of a tertiary care children's hospital and a provincial poison information centre. PATIENTS: The parents of 148 children who presented with vomiting completed the questionnaire. The database at the poison information centre included 474 reports of adverse drug reactions over an 8-year period and 105 reports of telephone inquiries over a 4-year period. MAIN RESULTS: Twenty-one (14%) of 148 children had received dimenhydrinate before arrival at the emergency department. The patients who had received dimenhydrinate were more likely than the others to present more than 12 hours after the onset of vomiting (14 [67%] of 21 v. 43 [34%] of 127, p less than 0.01). The discharge diagnoses for those who had received dimenhydrinate included asthma, pelvic inflammatory disease and urinary tract infection. No clinically important direct adverse reactions to dimenhydrinate were documented. CONCLUSIONS: The use of dimenhydrinate in children with vomiting is associated with a risk of delay in the diagnosis of treatable medical conditions.

Capsaicin inhibits calmodulin-mediated oxidative burst in rat macrophages.

In this study we seek to elucidate the interaction of capsaicin with the calmodulin mediated signal pathways in macrophages, by comparing its action on macrophage functions with a known calmodulin antagonist, fluphenazine. Kinetics of capsaicin uptake by macrophages (10(3) cells) revealed that a maximum of 200 microM capsaicin was taken up within 10 min. Ca2+ ionophore triggered generation of superoxide anion and hydrogen peroxide by macrophages was inhibited in a dose-dependent manner by fluphenazine (IC50, 20 microM and 12 microM, respectively) and also by capsaicin (IC50, 30 microM and 9 microM, respectively), suggesting an involvement of calmodulin in the regulation of NADPH oxidase. In vitro both fluphenazine and capsaicin inhibited Ca2(+)-Mg2+ ATPase and cAMP-phosphodiesterase from macrophages and this inhibition was reversed by exogenous addition of calmodulin. Fluorescence studies revealed a direct Ca2+ dependent interaction of capsaicin with calmodulin. From these results we suggest that capsaicin acts via calmodulin to inhibit stimulus-induced macrophage oxidative burst and also that calmodulin regulates the oxidative burst in macrophages.