Biomedical subjects

J Kurhanewicz

Publications and source records attributed to J Kurhanewicz.

43 records · Page 3Linked to original sources

PubMed1991

31P magnetic resonance spectroscopy (MRS) of experimental orbital myositis.

We described a model of orbital myositis that was induced by 12-0-tetradecanoyl-phorbol-13-acetate (TPA) injection into the superior rectus muscle of New Zealand white rabbits. In this study, in vivo 31P magnetic resonance spectroscopy (MRS) was performed with a 4.7 Tesla Oxford (Oxford Instruments, Oxford, England) magnet to monitor the evolution of muscle inflammation in control animals and the response of this model to external beam radiation. 31P MRS showed a dramatic increase in high-energy phosphorus and phospholipid metabolites 48 hr after TPA injection. These spectra were similar to those from implanted allogenic fibroblasts. Within 18-48 hr after a single dose (400 cGy) or sequential doses (3 days at 400 cGy) of orbital irradiation, reduced extraocular muscle swelling and a significant decrease of all 31P metabolites occurred. A decrease (63 +/- 6%) in the signal-to-noise (S/N) ratio of the control inflamed muscle 31P MR spectra increased by 28 days after inflammation. Two days after single-dose radiation, 31P MR metabolites were significantly lower (58 +/- 5%, P less than 0.012) than control spectra. These postradiation spectra mirror the 28-day control spectra and are consistent with previous histologic data that show decreased fibroblastic activity. Change in 31P MRS was a sensitive indicator of treatment response latency.

Animals↗

PubMed1990

Diffusion-weighted MR imaging of acute stroke: correlation with T2-weighted and magnetic susceptibility-enhanced MR imaging in cats.

We evaluated the temporal and anatomic relationships between changes in diffusion-weighted MR image signal intensity, induced by unilateral occlusion of the middle cerebral artery in cats, and tissue perfusion deficits observed in the same animals on T2-weighted MR images after administration of a nonionic intravascular T2 shortening agent. Diffusion-weighted images obtained with strong diffusion-sensitizing gradient strengths (5.6 gauss/cm, corresponding to gradient attenuation factor, b, values of 1413 sec/mm2) displayed increased signal intensity in the ischemic middle cerebral artery territory less than 1 hr after occlusion, whereas T2-weighted images without contrast usually failed to detect injury for 2-3 hr after stroke. After contrast administration (0.5-1.0 mmol/kg by Dy-DTPA-BMA, IV), however, T2-weighted images revealed perfusion deficits (relative hyperintensity) within 1 hr after middle cerebral artery occlusion that corresponded closely to the anatomic regions of ischemic injury shown on diffusion-weighted MR images. Close correlations were also found between early increases in diffusion-weighted MR image signal intensity and disrupted phosphorus-31 and proton metabolite levels evaluated with surface coil MR spectroscopy, as well as with postmortem histopathology. These data indicate that diffusion-weighted MR images more accurately reflect early-onset pathophysiologic changes induced by acute cerebral ischemia than do T2-weighted spin-echo images.

Acute Disease↗

PubMed1990

31P magnetic resonance spectroscopy of animal uveal melanoma.

Scleral surface coils were used to obtain in vivo magnetic resonance spectra (MRS) of Greene melanoma implanted in the rabbit uvea. Well-localized tumor spectra (4.7 Tesla) with good signal-to-noise ratios (S/N) were obtained from the tumor with a "single-pulse" sequence in less than 1 hour. Tumor localization was confirmed with one-dimensional spectroscopic imaging studies. Serial 31P spectra were obtained during tumor growth and after both optimal and suboptimal hyperthermia. Early 31P MRS change is correlated with tumor treatment response and preceded histologic evidence of cell destruction. Twenty-four to 48 hours after successful treatment, the inorganic phosphate/nucleoside triphosphate (NTP), and phosphomonoester/NTP ratios were significantly increased from 1.2 +/- 0.1 to 1.7 +/- 0.1 and 1.3 +/- 0.1 to 1.8 +/- 0.2, respectively. In contrast, untreated or ineffectively treated tumors showed little change. Interpretation of 31P MRS data in this animal uveal melanoma model after the first week was complicated by decreased S/N, increased contamination from contiguous tissues, ingrowth of fibroblasts, macrophages, and intratumor hemorrhage.

Animals↗

PubMed1989

MRS of ischemic/hypoxic brain disease.

Significant increases in magnetic field strengths and improvements in magnetic field homogeneity have made combined high-resolution magnetic resonance imaging (MRI) and multinuclear spectroscopy (MRS) feasible for investigating the relationship between biochemical and structural changes induced by ischemic brain disease. Magnetic resonance spectroscopy is the only noninvasive technique capable of measuring concentrations of high-energy phosphate metabolites, lactate, and other metabolically relevant compounds. Anticipated advances in localization of the volume of tissue from which spectra are obtained will enhance the clinical potential of MRS in the diagnosis of ischemic disease.

Animals↗

PubMedDate not supplied

Improved solvent suppression and increased spatial excitation bandwidths for three-dimensional PRESS CSI using phase-compensating spectral/spatial spin-echo pulses.

Dual phase-compensating spectral/spatial echo-planar (EP) spin-echo (SE) pulses were incorporated into the point resolved spectroscopy (PRESS) excitation sequence to improve water and lipid suppression for 1H chemical shift imaging (CSI) and to decrease the dependence of the PRESS box location upon chemical shift. The asymmetric EPSE pulses (either minimum or maximum phase in the chemical shift domain) were substituted for the two PRESS SE pulses to yield zero phase spectra. Three different pulses were designed and tested at 1.5 T. Pulse 1, targeted for brain CSI (TE > 85 msec), passed choline to lipid resonances, suppressed water, and rephased the methyl lactate doublet independently of TE. Pulse 2, targeted for general purpose shorter TE PRESS, possessed both high chemical shift and spatial domain bandwidths. Pulse 3, designed for prostate CSI, passed choline to citrate resonances while suppressing lipids and water. The three pulses possessed spatial bandwidths ranging between 3.3 and 5.0 kHz, more than three times higher than that offered by one-dimensional SE pulses of equivalent maximum B1 amplitude. Phantom and in vivo experimental results demonstrated that, for EPSE pulses 1 and 2, suppression factors higher than 10(4) were achieved. The increased spatial bandwidths resulted in less contamination by signals from outside the designated PRESS excited region and a significant improvement in the uniformity of metabolite intensities for voxels located near edges of the PRESS box.

Aged↗

PubMedDate not supplied

Phosphorus metabolite characterization of human prostatic adenocarcinoma in a nude mouse model by 31P magnetic resonance spectroscopy and high pressure liquid chromatography.

A series of experiments were conducted to identify and quantify the phosphorus metabolites of DU 145 xenografts (a human prostatic adenocarcinoma cell line grown in nude mice) using 31P MRS and HPLC. The 31P spectral characteristics of DU 145 xenografts were compared to perfused DU 145 cells and to in situ human prostatic adenocarcinomas. These studies demonstrated that both DU 145 xenografts and perfused DU 145 cells exhibited reduced levels of phosphocreatine relative to spectra of in situ human prostatic adenocarcinomas. Elevated levels of phosphomonesters (PMEs) were observed in 31P spectra of both DU 145 xenografts and in situ human prostatic adenocarcinomas. The major components of the PME resonance of DU 145 xenografts were identified as phosphocholine and phosphoethanolamine. High levels of diphosphodiesters (DPDEs) were consistently observed for both DU 145 xenografts and perfused DU 145 cells, but were absent in 31P spectra in in situ primary human adenocarcinomas. In agreement with spectroscopic results, high pressure liquid chromatographic analyses of human tissue removed at surgery contained insignificant amounts of DPDEs while DU 145 xenografts had high levels of DPDEs consisting mainly of uridine-5'-diphospho-N-acetylgalactosamine (22.4 nmol/mg protein) and uridine-5'-diphospho-N-acetylglucosamine (7.4 nmol/mg protein).

Adenocarcinoma↗

PubMedDate not supplied

Three-dimensional magnetic resonance spectroscopic imaging of brain and prostate cancer.

Clinical applications of magnetic resonance spectroscopic imaging (MRSI) for the study of brain and prostate cancer have expanded significantly over the past 10 years. Proton MRSI studies of the brain and prostate have demonstrated the feasibility of noninvasively assessing human cancers based on metabolite levels before and after therapy in a clinically reasonable amount of time. MRSI provides a unique biochemical "window" to study cellular metabolism noninvasively. MRSI studies have demonstrated dramatic spectral differences between normal brain tissue (low choline and high N-acetyl aspartate, NAA) and prostate (low choline and high citrate) compared to brain (low NAA, high choline) and prostate (low citrate, high choline) tumors. The presence of edema and necrosis in both the prostate and brain was reflected by a reduction of the intensity of all resonances due to reduced cell density. MRSI was able to discriminate necrosis (absence of all metabolites, except lipids and lactate) from viable normal tissue and cancer following therapy. The results of current MRSI studies also provide evidence that the magnitude of metabolic changes in regions of cancer before therapy as well as the magnitude and time course of metabolic changes after therapy can improve our understanding of cancer aggressiveness and mechanisms of therapeutic response. Clinically, combined MRI/MRSI has already demonstrated the potential for improved diagnosis, staging and treatment planning of brain and prostate cancer. Additionally, studies are under way to determine the accuracy of anatomic and metabolic parameters in providing an objective quantitative basis for assessing disease progression and response to therapy.

Brain Neoplasms↗