Knowledge of the 1 H magnetic properties of blood is important for developing models of the MR signal behavior in, for instance, the BOLD effect (1). Such models of free induction decay (FID) or spin echo (SE) experiments require accurate knowledge of the blood susceptibility and relaxation parameters as a function of blood oxygenation level. The blood signal is especially important in situations where the volume of interest contains large vessels and a major signal component arises directly from the MR behavior of bulk blood.It is widely assumed, and has been used in several modeling reports, that blood relaxation in the FID experiment can be described as pure Lorentzian behavior of the blood signal magnitude: S(t) ϰ exp(-R* 2 ⅐ t). It is shown herein that a substantial oxygenation-level-dependent non-Lorentzian component is an attribute of the bulk blood signal relaxation.As a note on nomenclature, the reader is reminded that exponential signal decay in the time domain (S(t) ϰ exp(-R* 2 ⅐ t)) leads to a Lorentzian lineshape (S() ϰ R* 2 / R* 2 2 ϩ 2 ) in the frequency domain. Herein we use the term "Lorentzian behavior" to describe frequency domain and time domain signal characteristics interchangeably. Likewise, Gaussian signal decay in the time domain (S(t) ϰ exp(-AR* ⅐ t 2 )) leads to a Gaussian lineshape (S() ϰ exp(-2 /4AR*)) in the frequency domain. As will be shown in this work, a Gaussian component arises in empirical modeling of the first 100 msec of the blood time domain signal magnitude. However, this is only a useful approximation. Time domain data demonstrate small (less than 2%) but significant systematic deviations from our empirical model, a simple product of Lorentzian and Gaussian components. To emphasize the fact that our empirical model does not fully account for the blood signal's relaxation characteristics (and that the model is not based on a biophysical model of blood magnetic properties) we use the generic phrase "non-Lorentzian signal behavior" to indicate as yet unexplained deviations from pure exponential/Lorentzian characteristics.Studies of the magnetic properties of human blood have been undertaken previously, and the results were insightful (2-13). However, as BOLD-related functional MRI (fMRI) procedures increase in precision, there is need to ensure the quantitative nature of the blood MR parameters upon which interpretation of experimental results may depend. Previous blood MR literature describes varying degrees of mismatch between the experimental conditions used for in vitro studies and human blood in situ. These differences include temperature (6,13,14), pH (13), and the settling of erythrocytes from plasma in the case of static samples (3,5-7,10 -12,14). Further, the relaxation rate constants in whole blood depend on magnetic field strength (3,6); hence it is important to determine these relaxation parameters at magnetic field strengths typical of human imaging systems.Of the in vitro studies cited herein, only two ensured a continuous mixing of the blood sample in order t...

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The metabolic state of skeletal muscle and brain within intact rats is monitored using high resolution phosphorus nuclear magnetic resonance. Regional disturbances in metabolism (for example, localised ischaemia) are easily observed, indicating the diagnostic possibilities of the method. Measurements are made using 'surface' radiofrequency coils, which we discuss in detail.

BACKGROUND Glyphosate-resistant (GR) weed species are now found with increasing frequency and threaten the critically importantGR weed management system. RESULTS The reported 31P NMR experiments on glyphosate-sensitive (S) and glyphosate-resistant (R) horseweed, Conyza canadensis (L.) Cronq., show significantly more accumulation of glyphosate within the R biotype vacuole. CONCLUSIONS Selective sequestration of glyphosate into the vacuole confers the observed horseweed resistance to glyphosate. This observation represents the first clear evidence for the glyphosate resistance mechanism in C. canadensis.

In the brain, on a macroscopic scale, diffusion of the intraneuronal constituent N-acetyl-L-aspartate (NAA) appears to be isotropic. In contrast, on a microscopic scale, NAA diffusion is likely highly anisotropic, with displacements perpendicular to neuronal fibers being markedly hindered, and parallel displacements less so. In this report we first substantiate that local anisotropy influences NAA diffusion in vivo by observing differing diffusivities parallel and perpendicular to human corpus callosum axonal fibers. We then extend our measurements to large voxels within rat brains. As expected, the macroscopic apparent diffusion coefficient (ADC) of NAA is practically isotropic due to averaging of the numerous and diverse fiber orientations. We demonstrate that the substantially non-monoexponential diffusion-mediated MR signal decay vs. b value can be quantitatively explained by a theoretical model of NAA confined to an ensemble of differently oriented neuronal fibers. On the microscopic scale, NAA diffusion is found to be strongly anisotropic, with displacements occurring almost exclusively parallel to the local fiber axis. This parallel diffusivity, ADC ʈ , is 0.36 ؎ 0.01 m 2 /ms, and ADC Ќ is essentially zero. From ADC ʈ the apparent viscosity of the neuron cytoplasm is estimated to be twice as large as that of a temperature-matched dilute aqueous solution.

A general statistical model that can describe a rather large number of experimental results related to the structure of the diffusion-attenuated MR signal in biological systems is introduced. The theoretical framework relies on a phenomenological model that introduces a distribution function for tissue apparent diffusion coefficients (ADC). It is shown that at least two parameters-the position of distribution maxima (ADC) and the distribution width ( )-are needed to describe the MR signal in most regions of a human brain. A substantial distribution width, on the order of 36% of the ADC, was found for practically all brain regions examined. This method of modeling the MR diffusion measurement allows determination of an intrinsic tissuespecific ADC for a given diffusion time independent of the strength of diffusion sensitizing gradients. Growing interest in diffusion MRI stems from numerous clinical and research applications (for example, see recent reviews in special issues of NMR in Biomedicine (1,2)). Most applications rely on a Stejskal-Tanner (3) pulsed gradient spin echo (PGSE) experiment and an assumption that the diffusion-attenuated MR signal can be expressed as a monoexponential function given by (3):Here ADC is the apparent diffusion coefficient for tissuewater or other MR active species under consideration; the so-called b-value depends on the shape of the diffusionsensitizing gradient pulse waveform G(t) (4):where ␥ is the magnetogyric (late gyromagnetic) ratio of the nuclide under consideration. For example (3), for the case of bipolar rectangular gradient pulses with amplitude G, duration ␦ and interval between pulse centers ⌬:[3]However, numerous studies of the diffusion of water and/or other metabolites in brain tissue and other biological systems have documented a non-monoexponential behavior of the MR signal S as a function of the b-value at fixed diffusion times (e.g., see Refs. 5-17). Most authors report that their data can be fit well by a biexponential function with two different diffusion coefficients (large/ fast and small/slow) and suggest ascribing the two exponential components to two physical compartments (extraand intracellular) in a tissue. However, as noted by Le Bihan and van Zijl (18), the origin of fast-and slow-diffusion pools is "still mysterious." Moreover, Sehy et al. (19) have directly observed biexponential diffusion MR signal behavior within the intracellular space of a single cell, the frog oocyte. Generally speaking, Eqs.[1] and [3] describe the diffusion-attenuated MR signal in a PGSE experiment only for unrestricted diffusion in homogeneous media. However, in most in vivo experiments each imaging or spectroscopic voxel contains numerous cells with different cell types, sizes, geometries, orientations, membrane permeabilities, and presumably different T 2 and T 1 relaxation time constants. Hence, the expectation that such a system can be described in terms of a simple unrestricted diffusion (monoexponential) model Eq. [1] is not reasonable. Practically any of the above-...

CorrectionsNEUROBIOLOGY. For the article ''Coupling between changes in human brain temperature and oxidative metabolism during prolonged visual stimulation'' by Dmitriy A. Yablonskiy, Joseph J. H. Ackerman, and Marcus E. Raichle, which appeared in number 13, June 20, 2000, of Proc. Natl. Acad. Sci. USA (97, 7603-7608), the authors note a correction in the second to last paragraph on page 7604. The sentence ''It is well known from positron-emission tomography (PET) data (17, 18) that rCMRO 2 maps in the normal human brain are largely flat despite considerable regional differences in rCBF and rCMRO 2 maps'' should read: ''It is well known from positron-emission tomography (PET) data (17,18) A fundamental discovery of modern human brain imaging with positron-emission tomography that the blood flow to activated regions of the normal human brain increases substantially more than the oxygen consumption has led to a broad discussion in the literature concerning possible mechanisms responsible for this phenomenon. Presently no consensus exists. It is well known that oxygen delivery is not the only function of systemic circulation. Additional roles include delivery of nutrients and other required substances to the tissue, waste removal, and temperature regulation. Among these other functions, the role of regional cerebral blood flow in local brain temperature regulation has received scant attention. Here we present a theoretical analysis supported by empirical data obtained with functional magnetic resonance suggesting that increase in regional cerebral blood flow during functional stimulation can cause local changes in the brain temperature and subsequent local changes in the oxygen metabolism. On average, temperature decreases by 0.2°C, but individual variations up to ؎1°C were also observed. Major factors contributing to temperature regulation during functional stimulation are changes in the oxygen consumption, changes in the temperature of incoming arterial blood, and extensive heat exchange between activated and surrounding brain tissue.

The biophysical mechanism(s) underlying diffusion-weighted MRI contrast following brain injury remains to be elucidated. Although it is generally accepted that water apparent diffusion coefficient (ADC) decreases after brain injury, it is unknown whether this is associated with a decrease in intracellular or extracellular water displacement, or both. To address this question, 2-[19F]luoro-2-deoxyglucose-6-phosphate (2FDG-6P) was employed as a compartment-specific marker in normal and globally ischemic rat brain. Through judicious choice of routes of administration, 2FDG-6P was confined to the intra- or extracellular space. There was no statistical difference between intra- and extracellular 2FDG-6P ADCs in normal or in globally ischemic brain (P > 0.16), suggesting that water ADCs in both compartments are similar. However, ischemia did result in a 40% ADC decrease in both compartments (P < 0.001). Assuming that 2FDG-6P reflects water motion, this study shows that water ADC decreases in both spaces after ischemia, with the reduction of intracellular water motion being the primary source of diffusion-weighted contrast.