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Biomedical subjects

J Beaumont

Publications and source records attributed to J Beaumont.

At least 19 recordsLinked to original sources
PubMed2005

A randomized phase II trial comparing every 3-weeks carboplatin/paclitaxel with every 3-weeks carboplatin and weekly paclitaxel in advanced non-small cell lung cancer.

BACKGROUND: The optimal schedule of taxane administration has been an area of active interest in several recent clinical trials. METHODS: To address a pure schedule question, we randomized 161 patients with advanced stage IIIB or IV non-small-cell lung cancer (NSCLC) to either paclitaxel 225 mg/m2 every 3 weeks x 4 cycles or 75 mg/m2/week x 12 (cumulative dose on each arm = 900 mg/m2). Both arms received concurrent carboplatin AUC 6 every 3 weeks x 4 cycles. RESULTS: The two arms were well-balanced in terms of known prognostic factors. The overall response rate and survival outcomes were similar on the two arms. There was significantly more grade 3/4 thrombocytopenia and grade 2-4 anemia on the weekly arm but less severe myalgias/arthralgias and alopecia. No difference in the rates of peripheral neuropathy was observed; however, patients on the every 3 weeks arm reported significantly more taxane therapy-related side-effects on the functional assessment of cancer therapy taxane subscale. CONCLUSIONS: This randomized trial exploring schedule-related issues with carboplatin/paclitaxel confirms the versatility of this regimen.

Adult↗
PubMed2001

Rectification of the background potassium current: a determinant of rotor dynamics in ventricular fibrillation.

Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. Yet, the mechanisms of VF remain elusive. Pixel-by-pixel spectral analysis of optical signals was carried out in video imaging experiments using a potentiometric dye in the Langendorff-perfused guinea pig heart. Dominant frequencies (peak with maximal power) were distributed throughout the ventricles in clearly demarcated domains. The fastest domain (25 to 32 Hz) was always on the anterior left ventricular (LV) wall and was shown to result from persistent rotor activity. Intermittent block and breakage of wavefronts at specific locations in the periphery of such rotors were responsible for the domain organization. Patch-clamping of ventricular myocytes from the LV and the right ventricle (RV) demonstrated an LV-to-RV drop in the amplitude of the outward component of the background rectifier current (I(B)). Computer simulations suggested that rotor stability in LV resulted from relatively small rectification of I(B) (presumably I(K1)), whereas instability, termination, and wavebreaks in RV were a consequence of strong rectification. This study provides new evidence in the isolated guinea pig heart that a persistent high-frequency rotor in the LV maintains VF, and that spatially distributed gradients in I(K1) density represent a robust ionic mechanism for rotor stabilization and wavefront fragmentation.

Animals↗
PubMed2000

A mechanism of transition from ventricular fibrillation to tachycardia : effect of calcium channel blockade on the dynamics of rotating waves.

Abbreviation of the action potential duration and/or effective refractory period (ERP) is thought to decrease the cycle length of reentrant arrhythmias. Verapamil, however, paradoxically converts ventricular fibrillation (VF) to ventricular tachycardia (VT), despite reducing the ERP. This mechanism remains unclear. We hypothesize that the size and the dynamics of the core of rotating waves, in addition to the ERP, influence the arrhythmia manifestation (ie, VF or VT). The objectives of this study were (1) to demonstrate functional reentry as a mechanism of VF and VT in the isolated Langendorff-perfused rabbit heart in the absence of an electromechanical uncoupler and (2) to elucidate the mechanism of verapamil-induced conversion of VF to VT. We used high-resolution video imaging with a fluorescent dye, ECG, frequency and 2-dimensional phase analysis, and computer simulations. Activation patterns in 10 hearts were studied during control, verapamil perfusion (2x10(-6) mol/L), and washout. The dominant frequency of VF decreased from 16.2+/-0.7 to 13.5+/-0.6 Hz at 20 minutes of verapamil perfusion (P<0.007). Concomitantly, phase analysis revealed that wavefront fragmentation was reduced, as demonstrated by a 3-fold reduction in the density of phase singularities (PSs) on the ventricular epicardial surface (PS density: control, 1.04+/-0.12 PSs/cm(2); verapamil, 0.32+/-0.06 PSs/cm(2) [P=0.0008]). On washout, the dominant frequency and the PS density increased, and the arrhythmia reverted to VF. The core area of transiently appearing rotors significantly increased during verapamil perfusion (control, 4.5+/-0.6 mm(2); verapamil, 9.2+/-0.5 mm(2) [P=0.0002]). In computer simulations, blockade of slow inward current also caused an increase in the core size. Rotating waves underlie VF and VT in the isolated rabbit heart. Verapamil-induced VF-to-VT conversion is most likely due to a reduction in the frequency of rotors and a decrease in wavefront fragmentation that lessens fibrillatory propagation away from the rotor.

Animals↗
PubMed2000

Vascular oxidant stress: molecular mechanisms and pathophysiological implications.

The term oxidative stress refers to a situation in which cells are exposed to excessive levels of either molecular oxygen or chemical derivatives of oxygen (ie, reactive oxygen species). Three enzyme systems produce reactive oxygen species in the vascular wall: NADH/NADPH oxidase, xanthine oxidoreductase, and endothelial nitric oxide synthase. Among vascular reactive oxygen species superoxide anion plays a critical role in vascular biology because it is the source for many other reactive oxygen species and various vascular cell functions. It is currently thought that increases in oxidant stress, namely excessive production of superoxide anion, are involved in the pathophysiology of endothelial dysfunction that accompanies a number of cardiovascular risk factors including hypercholesterolemia, hypertension and cigarette smoking. On the other hand, vascular oxidant stress plays a pivotal role in the evolution of clinical conditions such as atherosclerosis, diabetes and heart failure.

Animals↗
PubMed1999

Losartan inhibits the post-transcriptional synthesis of collagen type I and reverses left ventricular fibrosis in spontaneously hypertensive rats.

OBJECTIVE: Previous studies have shown that as well as left ventricular hypertrophy, myocardial fibrosis develops early in rats with spontaneous hypertension (SHR). The present study was designed to investigate whether chronic treatment with the angiotensin II type 1 (AT1) receptor antagonist losartan modifies collagen type I metabolism and reverses left ventricular fibrosis in young SHR with left ventricular hypertrophy. DESIGN: The study was performed in 30-week-old normotensive Wistar-Kyoto (WKY) rats, untreated SHR and SHR treated with losartan (20 mg/mg per day, orally) for 14 weeks before they were killed. METHODS: Ventricular pro-alpha 1 (I) collagen messenger RNA was analyzed by Northern blot. Serum levels of the carboxy-terminal propeptide of procollagen type I (PIP) and the pyridoline cross-linked telopeptide domain of collagen type I (CITP) were determined by specific radioimmunoassays as markers of collagen type I synthesis and degradation, respectively. Collagen volume fraction was determined in the left ventricle by quantitative morphometry. RESULTS: Compared with WKY rats, SHR exhibited increased (P < 0.05) mean arterial pressure, pro-alpha 1 (I) collagen messenger RNA, PIP and left ventricular collagen volume fraction, and similar CITP values. After the treatment period, mean arterial pressure was higher (P < 0.05) in losartan-treated SHR than in WKY rats. Compared with untreated SHR, treated SHR showed no left ventricular hypertrophy and diminished (P < 0.05) values of mean arterial pressure, PIP and left ventricular collagen volume fraction. No changes in pro-alpha 1 (I) collagen messenger RNA and CITP values were observed with treatment in SHR. No significant differences in the left ventricular collagen volume fraction were observed between treated SHR with normal blood pressure and treated SHR with abnormally high blood pressure at the end of the treatment period. CONCLUSIONS: These results suggest that chronic AT1 blockade with losartan decreases the post-transcriptional synthesis of fibril-forming collagen type I molecules in young SHR. This effect may be involved in the ability of this drug to reverse left ventricular fibrosis in young rats with genetic hypertension. Apart from its antihypertensive action, other mechanisms may mediate the antifibrotic effect of losartan in this animal model.

Animals↗
PubMed1998

Sound generation in gradient coil structures for MRI.

When supporting plates of plastic material are subjected to alternating transverse Lorentz forces while in a strong magnetic field normal to the plate surface, compressional waves within the solid produce a modulation of the plate surface that launches an acoustic wave in air along the magnetic field axis. We have extended our previous theory describing this process to include a detailed description of the formation of an acoustic interference pattern in air described by Fraunhofer diffraction at a distance from the plate surface. The extended theory predicts that the observed acoustic signal midpoint and normal to the plate surface gives a variation with frequency in approximate agreement with our previous measurements. The acoustic output off axis shows acoustic blazing that produces two main diffraction peaks with a splitting inversely proportional to the velocity of sound in the plate material. The new results could have important ramifications for the minimization of sound output in gradient coil design for MRI. A new arrangement of coils is proposed to ameliorate the acoustic output problem centrally and normal to the plate by extending the frequency response of the supporting plates to much higher frequencies. Also presented are estimates of the compressional wave velocities deduced from frequency response data recorded at the center-point of a number of different plates.

Magnetic Resonance Imaging↗
PubMed1998

Spiral waves in two-dimensional models of ventricular muscle: formation of a stationary core.

Previous experimental studies have clearly demonstrated the existence of drifting and stationary electrical spiral waves in cardiac muscle and their involvement in cardiac arrhythmias. Here we present results of a study of reentrant excitation in computer simulations based on a membrane model of the ventricular cell. We have explored in detail the parameter space of the model, using tools derived from previous numerical studies in excitation-dynamics models. We have found appropriate parametric conditions for sustained stable spiral wave dynamics (1 s of activity or approximately 10 rotations) in simulations of an anisotropic (ratio in velocity 4:1) cardiac sheet of 2 cm x 2 cm. Initially, we used a model that reproduced well the characteristics of planar electrical waves exhibited by thin sheets of sheep ventricular epicardial muscle during rapid pacing at a cycle length of 300 ms. Under these conditions, the refractory period was 147 ms; the action potential duration (APD) was 120 ms; the propagation velocity along fibers was 33 cm/s; and the wavelength along fibers was 4.85 cm. Using cross-field stimulation in this model, we obtained a stable self-sustaining spiral wave rotating around an unexcited core of 1.75 mm x 7 mm at a period of 115 ms, which reproduced well the experimental results. Thus the data demonstrate that stable spiral wave activity can occur in small cardiac sheets whose wavelength during planar wave excitation in the longitudinal direction is larger than the size of the sheet. Analysis of the mechanism of this observation demonstrates that, during rotating activity, the core exerts a strong electrotonic influence that effectively abbreviates APD (and thus wavelength) in its immediate surroundings and is responsible for the stabilization and perpetuation of the activity. We conclude that appropriate adjustments in the kinetics of the activation front (i.e., threshold for activation and upstroke velocity of the initiating beat) of currently available models of the cardiac cell allow accurate reproduction of experimentally observed self-sustaining spiral wave activity. As such, the results set the stage for an understanding of functional reentry in terms of ionic mechanisms.

Action Potentials↗
PubMed1998

Altered regulation of smooth muscle cell proliferation and apoptosis in small arteries of spontaneously hypertensive rats.

AIM: It has been proposed that alterations of the balance between programmed cell death and cell replication might be involved in abnormalities of smooth muscle cell growth in arterial hypertension. This study was designed to analyse some regulators of apoptosis and proliferation in smooth muscle cells of small intra-myocardial arteries from the left ventricle of adult normotensive Wistar-Kyoto rats (WKY) and adult spontaneously hypertensive rats (SHR). Therefore, we assessed the expression of the cytoplasmic proteins Bax and Bcl-2, respectively a promoter and an inhibitor of apoptosis, and the expression of cyclin A, a nuclear protein that induces proliferation of smooth muscle cells. METHODS AND RESULTS: We measured the percentages of smooth muscle cells expressing these proteins using monoclonal antibodies and the avidin-biotin immunoperoxidase method. Compared with WKY, cells from SHR exhibited normal Bax expression, increased (P < 0.001) Bcl-2 expression and increased (P < 0.001) cyclin A expression. The ratio of Bax to Bcl-2, an index of cell susceptibility to apoptosis, was lower (P < 0.001) in SHR than in WKY. Systolic blood pressure was directly correlated (P < 0.01) with Bcl-2 and cyclin A in SHR. CONCLUSION: These results suggest that apoptosis and proliferation of smooth muscle cells might be inhibited and stimulated, respectively, in small arteries of adult SHR. The imbalance between these two processes may account for abnormalities of smooth muscle cell growth in the arterial wall in genetic hypertension.

Animals↗
PubMed1996

AV nodal function during atrial fibrillation: the role of electrotonic modulation of propagation.

The irregular ventricular rhythm that accompanies atrial fibrillation (AF) has been explained in terms of concealed conduction within the AV node (AVN). However, the cellular basis of concealed conduction in AF remains poorly understood. Our hypothesis is that electrotonic modulation of AVN propagation by atrial impulses blocked repetitively within the AVN is responsible for changes in function that lead to irregular ventricular rhythms in patients with AF. We have tested this idea using two different simplified computer ionic models of the AVN. The first ("black-box") model consisted of three cells: one representing the atrium, another one representing the AVN, and a third one representing the ventricle. The black-box model was used to establish the rules of behavior and predictions to be tested in a second, more elaborate model of the AVN. The latter ("nine-cell" model) incorporated a linear array of nine cells separated into three different regions. The first region of two cells represented the atrium; the second region of five cells represented the AV node; and the third region of two cells represented the ventricle. Cells were connected by appropriate coupling resistances. During regular atrial pacing, both models reproduced very closely the frequency dependence of AV conduction and refractoriness seen in patients and experimental animals. In addition, atrial impulses blocked within the AV node led to electrotonic inhibition or facilitation of propagation of immediately succeeding impulses. During simulated AF, using the nine-cell model, random variations in the atrial (A-A) interval yielded variations in the ventricular (V-V) interval but there was no scaling, i.e., the V-V intervals were not multiples of the A-A intervals. As such, the model simulated the statistical behavior of the ventricles in patients with AF, including: (1) the ventricular rhythm was random; and (2) the coefficient of variation (standard deviation/mean) of the ventricular rhythm was relatively constant at any given mean V-V interval. Analysis of cell responses revealed that repetitive atrial input at random A-A intervals resulted in complex patterns of concealment within the AVN cells. Consequently, the effects of electrotonic modulation were also random, which resulted in a smearing of the AV conduction curve over A-A intervals that were larger than those predicted for 1:1 AV conduction. Hence, during AF, electrotonic modulation acts in concert with the frequency dependence of AVN conduction to result in complex patterns of ventricular activation. Finally, similarly to what was shown in patients, VVI pacing of the ventricle in the nine-cell model at the appropriate frequency led to blockade of nearly all anterograde (i.e., A-V) impulses. The essential feature here was that the retrograde impulse invading the AVN cells was followed by refractoriness with slow recovery of excitability, setting the stage for electrotonic inhibition of anterograde impulses. Overall, the results provide insight into the cellular mechanisms underlying AVN function and irregular ventricular response during AF.

Animals↗
PubMed1995

A model study of changes in excitability of ventricular muscle cells: inhibition, facilitation, and hysteresis.

A model study was carried out to investigate the mechanism of changes in excitability at long cycle lengths (i.e., > 1,000 ms), which are responsible for various phenomena, including electrotonic inhibition, active facilitation, and hysteresis of excitability in ventricular muscle at slow frequencies of stimulation. Experimental studies suggested that with repetitive activity the inward rectifier potassium current (IK1) is not a passive component of membrane response and that the dynamics of IK1 are responsible for the changes in excitability at long cycle lengths. In the present study, we have used new experimental data as the basis to modify the equations for IK1 in the ionic model for ventricular muscle of the Luo and Rudy (LR) model. The modified equations for IK1 incorporate an additional slow gate (s-gate), which governs the transition from a high steady-state conductance at rest to a lower conductance with repetitive stimulation. In simulation studies, electronic inhibition was seen in the original and the modified LR model and was shown to depend on changes in the delayed rectifier current (IK). However, addition of the s-gate to IK1 of the LR model extended the frequency dependence of excitability to longer cycle lengths and allowed for the demonstration of active facilitation and hysteresis. These results support the hypothesis that the inward rectifier is involved in the dynamic control of membrane excitability. The overall results provide mechanistic explanations for heart rate-dependent excitation abnormalities that may be involved in the genesis of cardiac arrhythmias.

Algorithms↗
PubMed1994

Electrotonic inhibition and active facilitation of excitability in ventricular muscle.

INTRODUCTION: The effects of subthreshold electrical pulses on the response to subsequent stimulation have been described previously in experimental animal studies as well as in the human heart. In addition, previous studies in cardiac Purkinje fibers have shown that diastolic excitability may decrease after activity (active inhibition) and, to a lesser extent, following subthreshold responses (electrotonic inhibition). However, such dynamic changes in excitability have not been explored in isolated ventricular muscle, and it is uncertain whether similar phenomena may play any role in the activation patterns associated with propagation abnormalities in the myocardium. METHODS AND RESULTS: Experiments were performed in isolated sheep Purkinje fibers and papillary muscles, and in enzymatically dissociated guinea pig ventricular myocytes. In all types of preparations introduction of a conditioning subthreshold pulse between two suprathreshold pulses was followed by a transient decay in excitability (electrotonic inhibition). The degree of inhibition was directly related to the amplitude and duration of the conditioning pulse and inversely related to the postconditioning interval. Yet, inhibition could be demonstrated long after (> 1 sec) the end of the conditioning pulse. Electronic inhibition was found at all diastolic intervals and did not depend on the presence of a previous action potential. In Purkinje fibers, conditioning action potentials led to active inhibition of subsequent responses. In contrast, in muscle cells, such action potentials had a facilitating effect (active facilitation). Electrotonic inhibition and active facilitation were observed in both sheep ventricular muscle and guinea pig ventricular myocytes. Accordingly, during repetitive stimulation with pulses of barely threshold intensity, we observed: (1) bistability (i.e., with the same stimulating parameters, stimulus:response patterns were either 1:1 or 1:0, depending on previous history), and (2) abrupt transitions between 1:1 and 1:0 (absence of intermediate Wenckebach-like patterns). Simulations utilizing an ionic model of cardiac myocytes support the hypothesis that electrotonic inhibition in well-polarized ventricular muscle is the result of partial activation of IK following subthreshold pulses. On the other hand, active facilitation may be the result of an activity-induced decrease in the conductance of IK1. CONCLUSION: Diastolic excitability of well-polarized ventricular myocardium may be transiently depressed following local responses and transiently enhanced following action potentials. On the other hand, diastolic excitability decreases during quiescence. Active facilitation and electrotonic inhibition may have an important role in determining the dynamics of excitation of the myocardium in the presence of propagation abnormalities.

Action Potentials↗
PubMed1993

On the interpretation of voltage-clamp data using the Hodgkin-Huxley model.

This paper describes a method to extract membrane model parameters from experimental voltage-clamp records. The underlying theory is based on two premises: (1) the membrane dynamics can be described by a Hodgkin-Huxley (HH) model, and (2) the most reliable data provided by voltage clamp experiments are peak current (Ip) measurements. First, the steady-state characteristics of activation (x infinity) and inactivation (z infinity) must be estimated, and it is shown that Ip data provided by standard voltage-clamp stimulation protocols are sufficient for this purpose for the case of well-separated activation (tau x) and inactivation (tau z) time constants, tau x << tau z. Next, we propose a test (R test) to establish the suitability of the HH model to represent the data. When the HH model is applicable (successful R test), the procedure yields the degree of the gating variables, a range of maximum membrane conductance (g) values, and a tau x/tau z ratio that relates x infinity and z infinity to the Ip data. When additional information is available, such as the time of occurrence of Ip or an estimate of tau z from the late portion of the ionic current response, one can narrow down the value of g and estimate all the HH parameters and functions. Otherwise, when the R test is not successful, one can conclude that x infinity and z infinity have been incorrectly estimated because tau x and tau z are not sufficiently separated or that the HH model is not applicable to the data.

Algorithms↗
PubMed1993

Estimation of the steady-state characteristics of the Hodgkin-Huxley model from voltage-clamp data.

In a companion paper in this issue we show that all the parameters and functions of the Hodgkin-Huxley (HH) model can be calculated in a unique and optimal manner from voltage-clamp peak current data when the steady-state activation (x infinite) and inactivation (z infinite) characteristics are known. Assuming that x infinite and z infinite can be adequately expressed by a Boltzmann equation with two parameters, the present paper describes an optimization procedure to estimate these parameters from peak current data without any constraint on the time constants of activation and inactivation. The required voltage-clamp data are the peak ionic current value (Ip) and its time of occurrence (tp), as provided by two complementary voltage-clamp protocols involving, in each case, a single fixed value of clamp potential. The performance of the procedure was very good with simulated medium- or high-resolution data as it was then possible to determine with confidence the degrees of the gating variables. The performance was also very good with low-resolution data, provided that the degrees of the gating variables were chosen correctly. Good results were also obtained in the presence of Gaussian noise. On the other hand, estimates of x infinite and z infinite based on normalization of peak current measurements always give uncertain results that are likely to be incorrect in a number of circumstances. It is concluded that the HH model can be a useful tool for the interpretation of voltage-clamp peak current data when a reasonable database is available.

Animals↗
PubMed1992

Phenylethylamine and piperidine alkaloids in aloe species.

Of the approximately 300 species of ALOE (Liliaceae) native to Africa and Arabia, leaf extracts of 224 species have been examined chromatographically for alkaloids using ninhydrin, Dragendorff's reagent, nitroprusside, and iodoplatinate as revealing agents. From these, 48 (21%) species contained compounds giving a strong colorimetric reaction with at least one of these reagents. Tyramine derivatives were identified in 18 species and piperidine derivatives in a further 6 species. The other coloured zones remain unidentified but often appeared to represent common amino acids. Some taxonomic correlations are suggested. The presence of the toxic hemlock alkaloids in aloes readily available for potential medicinal use by local inhabitants sounds a note of caution against the unthinking use of these otherwise useful plants.

Journal Article↗
PubMed1992

Intracellular regulation of cell adhesion to extracellular matrix components in murine B16 melanoma cells.

The involvement of signal transduction systems in the initial attachment of two murine B16 melanoma clones of differing metastatic potential to extracellular matrix components was examined to learn more of the early events in cell-matrix interaction. Clones of high and low metastatic capacity attached similarly in the absence of any stimulators, exhibiting a two phase time course of attachment with 100% attachment by 60 min. A slight difference in attachment characteristics between the clones was seen in response to phorbol ester stimulation, which significantly inhibited attachment of the low metastatic clone but which had no effect on the highly metastatic clone. Total protein kinase C activity and distribution was similar for both clones. Attachment of both clones was severely reduced, however, if intracellular calcium was elevated or intracellular calmodulin inhibited. This study suggests that signal transduction mechanisms are involved in melanoma cell attachment to matrix proteins and offers an approach to pharmacological manipulation of these cell-matrix interactions which may be relevant to reducing metastatic spread.

Animals↗
PubMed1991

Lung cancer in mild steel welders.

To investigate lung cancer risk, the authors conducted a historical cohort mortality study of 4,459 mild steel welders who had been employed at three midwestern plants which manufactured heavy equipment. Follow-up began in the mid-1950s and extended through 1988. All welders had at least 2 years welding experience (average duration, 8.5 years). This cohort had no occupational exposure to asbestos or stainless steel fumes (containing nickel and chromium), two potential confounders in previous welders studies. A comparison population of 4,286 nonwelders, all with at least 2 years employment at the same plants, was also studied. Nonwelders had never been welders and were allowed to have no more than 90 days employment as a painter, foundryman, or machinist. Sampling data collected from 1974-1987 indicated that welders were exposed to 6-7 mg/m3 of total particulate and 3-4 mg/m3 of iron oxide, while nonwelders had negligible exposures to welding fumes. When compared with the United States population, both welders and nonwelders had elevated rates for lung cancer (standardized mortality ratios (SMRs): welders, SMR = 1.07; nonwelders, SMR = 1.17), but neither SMR was significantly elevated. Limited smoking data based on a 1985 survey indicated that both welders and nonwelders smoked more than the United States population, possibly accounting for part of their elevated lung cancer rates. There was no trend of increased risk for welders with increased duration of exposure. The only other cause of death significantly elevated was emphysema among welders. Nonmalignant respiratory disease was not elevated for welders (SMR = 0.96). When welders were compared with nonwelders directly for lung cancer, the rate ratio was 0.90.

Cause of Death↗
PubMed1991

Magnetic resonance imaging.

Magnetic Resonance Imaging is the latest diagnostic tool to have a significant impact on patient management. Magnetic Resonance Imaging, or MRI, has been available for over six years but has only in the last 18 months become readily available to many more hospitals in Great Britain. MRI scanners have been purchased by large specialist hospitals but the arrival of mobile MRI scanners has made the technology available to smaller hospitals and groups. The impact of MRI for all clinicians and especially surgeons is great and the following text will outline the advantages of MRI and mobile MRI.

Humans↗