Increase In T2 Values Research Articles

Challenges towards MR imaging of the peripheral inflammatory response in the subacute and chronic stages of transient focal ischemia

Intravenous administration of iron oxide nanoparticles after experimental stroke has been shown to produce focal signal intensity changes in the ischemic boundary on MRI images. These changes have been attributed to the influx of iron-laden blood-borne macrophages, although it has been suggested that this effect might not always be completely specific to inflammatory cells. The aim of the present study was to investigate this phenomenon in a subacute time frame that is more relevant to the peripheral inflammatory response. Imaging experiments (T(2) -, T(2)*- and T(1) -weighted sequences) were acquired in Wistar rats 6 days after transient middle cerebral artery occlusion (MCAO). Animals were intravenously infused with different doses of ultrasmall superparamagnetic iron oxide (USPIO) nanoparticles (300, 600 or 1000 µmol Fe/kg), or saline and gadolinium, and imaged again 24 h later. Tissue was immediately processed for immunohistochemistry with the macrophage marker ED-1, in combination with Prussian blue for iron. Ischemic tissue exhibited a large increase in T(2) values, and overall contrast enhancement was apparent in the brain and surrounding muscle. In contrast with previous reports, there were no regions of focal signal intensity changes in the ischemic territory in any of the images, although a region of interest analysis revealed a trend towards iron accumulation in the ischemic hemisphere, particularly in the cortex of T(2)* images. However, histological examination revealed that, despite extensive ED-1-positive macrophage accumulation in the entire ischemic territory, none of these cells were Prussian blue positive, except in the meninges of one animal that received a high dose of USPIO nanoparticles. These results imply that the observed trend is a result of the presence of contrast agent in the blood, or meninges, and not iron-containing inflammatory cells.

Nuclear magnetic resonance water relaxation time changes in bananas during ripening: a new mechanism

Nuclear magnetic resonance studies of banana fragments during ripening show an increase on the water transverse relaxation time (T2) and a decrease in water self-diffusion coefficient (D). As T(2) and D are normally directly correlated, we studied these two properties in intact bananas during ripening, in an attempt to rule out the effect of injury on the apparent discrepancies in the behavior of T(2) and D. The results show that injury in bananas causes a decrease in T2 of the water in vacuoles (T(2vac)). They also show that T(2vac) increased and D decreased during ripening, ruling out the injury effect. To explain the apparent discrepancies, we propose a new hypothesis for the increase in T2 values, based on the reduction of Fe3+ ions to Fe2+ by galacturonic acid, produced by the hydrolysis of pectin and a decrease in internal oxygen concentration during ripening. As injury alters T2 values it is necessary to use intact bananas to study relaxation times during ripening. The novel interpretation for the increase in T(2vac) based on reduction of Fe+3 and O2 concentration is an alternative mechanism to that based on the hydrolysis of starch in amyloplasts.

Evaluation and comparison of cartilage repair tissue of the patella and medial femoral condyle by using morphological MRI and biochemical zonal T2 mapping

The objective of this study was to use advanced MR techniques to evaluate and compare cartilage repair tissue after matrix-associated autologous chondrocyte transplantation (MACT) in the patella and medial femoral condyle (MFC). Thirty-four patients treated with MACT underwent 3-T MRI of the knee. Patients were treated on either patella (n = 17) or MFC (n = 17) cartilage and were matched by age and postoperative interval. For morphological evaluation, the MR observation of cartilage repair tissue (MOCART) score was used, with a 3D-True-FISP sequence. For biochemical assessment, T2 mapping was prepared by using a multiecho spin-echo approach with particular attention to the cartilage zonal structure. Statistical evaluation was done by analyses of variance. The MOCART score showed no significant differences between the patella and MFC (p > or = 0.05). With regard to biochemical T2 relaxation, higher T2 values were found throughout the MFC (p < 0.05). The zonal increase in T2 values from deep to superficial was significant for control cartilage (p < 0.001) and cartilage repair tissue (p < 0.05), with an earlier onset in the repair tissue of the patella. The assessment of cartilage repair tissue of the patella and MFC afforded comparable morphological results, whereas biochemical T2 values showed differences, possibly due to dissimilar biomechanical loading conditions.

Magnetic Resonance Imaging Detects and Predicts Early Brain Injury after Subarachnoid Hemorrhage in a Canine Experimental Model

The canine double hemorrhage model is an established model to study cerebral vasospasm, the late sequelae of subarachnoid hemorrhage (SAH). The present study uses magnetic resonance imaging (MRI) to examine the recently reported early brain injury after SAH. Double hemorrhage SAH modeling was obtained by injecting 0.5 mL/kg of autologous arterial blood into the cisterna magna of five adult mongrel dogs on day 0 and day 2, followed by imaging at day 2 and day 7 using a 4.7-Tesla (T) scanner. White matter (WM) showed a remarkable increase in T2 values at day 2 which resolved by day 7, whereas gray matter (GM) T2 values did not resolve. The apparent diffusion coefficient (ADC) values progressively increased in both WM and GM after SAH, suggestive of a transition from vasogenic to cytotoxic edema. Ventricular volume also increased dramatically. Prominent neuronal injury with Nissl's staining was seen in the cortical GM and in the periventricular tissue. Multimodal MRI reveals acute changes in the brain after SAH and can be used to non-invasively study early brain injury and normal pressure hydrocephalus post-SAH. MR can also predict tissue histopathology and may be useful for assessing pharmacological treatments designed to ameliorate SAH.

Apparent Diffusion Coefficient Reveals Gray and White Matter Disease, and T2 Mapping Detects White Matter Disease in the Brain in Feline Alpha-Mannosidosis

Methods to locate and identify brain pathology are critical for monitoring disease progression and for evaluating the efficacy of therapeutic intervention. The purpose of this study was to detect cell swelling, abnormal myelin, and astrogliosis in the feline model of the lysosomal storage disease alpha-mannosidosis (AMD) by using diffusion and T2 mapping. Average apparent diffusion coefficient (ADC(av)) and T2 were measured by imaging the brains of five 16-week-old cats with feline AMD on a 4.7T magnet. ADC(av) and T2 data from affected cats were compared with data from age-matched normal cats. Brains were collected from both affected and normal cats following imaging, and histology was compared with quantitative imaging data. Gray matter from AMD cats demonstrated a 13%-15% decrease in ADC(av) compared with that in normal cats. White matter from AMD cats exhibited an 11%-16% decrease in ADC(av) and a 5%-12% increase in T2 values compared with those in normal control cats. Histologic evidence of neuronal and glial swelling, abnormal myelin, and astrogliosis was consistent with changes in ADC(av) and T2. ADC(av) and T2 data can be used to quantify differences in the gray and white matter in the feline AMD brain and may serve as surrogate markers of neuronal swelling, abnormal myelin, and astrogliosis associated with this disease. These studies may be helpful in assessing the efficacy of experimental therapies for central nervous system disease associated with lysosomal storage diseases.

Abstracts of literature

Abstracts of literature

Secondary decline in apparent diffusion coefficient and neurological outcomes after a short period of focal brain ischemia in rats

This study was designed to characterize the initial and secondary changes of the apparent diffusion coefficient (ADC) of water with high temporal resolution measurements of ADC values and to correlate ADC changes with functional outcomes. Fourteen rats underwent 30 minutes of temporary middle cerebral artery occlusion (MCAO). Diffusion-, perfusion-, and T2-weighted imaging was performed during MCAO and every 30 minutes for a total of 12 hours after reperfusion (n = 6). Neurological outcomes were evaluated during MCAO, every 30 minutes for a total of 6 hours and at 24 hours after reperfusion (n = 8). The decreased cerebral blood flow during MCAO returned to normal after reperfusion and remained unchanged thereafter. The decreased ADC values during occlusion completely recovered at 1 hour after reperfusion. The renormalized ADC values started to decrease secondarily at 2.5 hours, accompanied by a delayed increase in T2 values. The ADC-defined secondary lesion grew over time and was 52% of the ADC-defined initial lesion at 12 hours. Histological evaluation demonstrated neuronal damage in the regions of secondary ADC decline. Complete resolution of neurological deficits was seen in 1 rat at 1 hour and in 6 rats between 2.5 and 6 hours after reperfusion; no secondary neurological deficits were observed at 24 hours. These data suggest that (1) a secondary ADC reduction occurs as early as 2.5 hours after reperfusion, evolves in a slow fashion, and is associated with neuronal injury; and (2) renormalization and secondary decline in ADC are not associated with neurological recovery and worsening, respectively.

Secondary decline in apparent diffusion coefficient and neurological outcomes after a short period of focal brain ischemia in rats

This study was designed to characterize the initial and secondary changes of the apparent diffusion coefficient (ADC) of water with high temporal resolution measurements of ADC values and to correlate ADC changes with functional outcomes. Fourteen rats underwent 30 minutes of temporary middle cerebral artery occlusion (MCAO). Diffusion-, perfusion-, and T2-weighted imaging was performed during MCAO and every 30 minutes for a total of 12 hours after reperfusion (n = 6). Neurological outcomes were evaluated during MCAO, every 30 minutes for a total of 6 hours and at 24 hours after reperfusion (n = 8). The decreased cerebral blood flow during MCAO returned to normal after reperfusion and remained unchanged thereafter. The decreased ADC values during occlusion completely recovered at 1 hour after reperfusion. The renormalized ADC values started to decrease secondarily at 2.5 hours, accompanied by a delayed increase in T2 values. The ADC-defined secondary lesion grew over time and was 52% of the ADC-defined initial lesion at 12 hours. Histological evaluation demonstrated neuronal damage in the regions of secondary ADC decline. Complete resolution of neurological deficits was seen in 1 rat at 1 hour and in 6 rats between 2.5 and 6 hours after reperfusion; no secondary neurological deficits were observed at 24 hours. These data suggest that (1) a secondary ADC reduction occurs as early as 2.5 hours after reperfusion, evolves in a slow fashion, and is associated with neuronal injury; and (2) renormalization and secondary decline in ADC are not associated with neurological recovery and worsening, respectively. Ann Neurol 2000;48:236–244

Relaxation Times of Normal Breast Tissues

The influence of age on the relaxation times of normal breast parenchyma and its surrounding fatty tissue were evaluated, and the variations during a normal menstrual cycle were analyzed using an ultra low field 0.02 T imager. Thirty-nine healthy volunteers aged 21 to 59 years were examined to determine T1 and T2 relaxation times, and 8 of these volunteers were studied once weekly during one menstrual cycle. The only significant trend was an increase in the T2 of breast parenchyma with increasing age. During the menstrual cycle there was a slight but insignificant (p = 0.10) increase in T1 of the breast parenchyma values during the latter half of the menstrual cycle, and a corresponding increase in T2 values between the 2nd and 3rd weeks of the menstrual cycle, which was significant (p = 0.003).

Relaxation times of normal breast tissues

The influence of age on the relaxation times of normal breast parenchyma and its surrounding fatty tissue were evaluated, and the variations during a normal menstrual cycle were analyzed using an ultra low field 0.02 T imager. Thirty-nine healthy volunteers aged 21 to 59 years were examined to determine T1 and T2 relaxation times, and 8 of these volunteers were studied once weekly during one menstrual cycle. The only significant trend was an increase in the T2 of breast parenchyma with increasing age. During the menstrual cycle there was a slight but insignificant (p = 0.10) increase in T1 of the breast parenchyma values during the latter half of the menstrual cycle, and a corresponding increase in T2 values between the 2nd and 3rd weeks of the menstrual cycle, which was significant (p = 0.003).

Proton magnetic resonance of early myocardial infarction in rats.

In vitro (10 MHz) proton magnetic resonance (MR) was used to study myocardial infarction 30 hours after ligation of the left coronary artery in rats. The location of large anterolateral myocardial wall infarcts was confirmed when the rats were killed. In vitro measurements of control animals (n = 7) showed T1 prolongation in right as compared with left ventricles (559 +/- 41 vs. 522 +/- 35 milliseconds [sd]; P less than .02); this correlated with a higher water content and is believed to be caused by increased extracellular compartment size. Infarcted myocardium (n = 9) had lower T1 relaxation times than control left ventricle anterior walls (480 +/- 37 vs. 522 +/- 35 milliseconds; P less than .01) despite increased water content (78 +/- 1.1% vs. 76.5 +/- 6%; P less than .01) and a mild increase in T2 values. We conclude that the MR characteristics of myocardial infarction in rats differ from those of other models, possibly because of differences in infarct sizes and rates of proteolysis within the damaged tissues.

Proton Relaxation Times in Bleomycin-Induced Lung Injury

Pulmonary fibrosis and inflammation induced in mice by biweekly injection of low doses (20 mg/kg) of bleomycin chronically administered subcutaneously was associated with a significant increase in T2 values measured in vitro (54.6 +/- 20.7 ms vs. 36.2 +/- 3.8 ms in controls). T1 values, however, were not altered significantly (613 +/- 124.6 ms vs. 666 +/- 105.7 ms in controls). Lung water content did not change (79.1 +/- 2.5% vs. 78.4 +/- 0.98% in controls, NS). Water content to dry weight ratio in the control group (3.63 +/- 0.212) did not differ significantly from that in the experimental group clinically treated with bleomycin (3.84 +/- .618). However, morphometric and histologic analysis indicated that in 71% of the chronically treated mice, there was marked pulmonary fibrosis (mean area of involvement 3.5 +/- 8.1% vs. 0.25 +/- 0.15% in controls, P less than .01). In addition, there was marked increase in pulmonary cellularity and infiltration by lymphocytes and macrophages (mean area of macrophage infiltration 8.71 +/- 13.256% vs. 1.17 +/- 1.404% in controls). The alteration in T2 in bleomycin damaged lung occurred in the absence of change in overall water content. However, the change in cellularity indicates an alteration of water distribution between the cellular, intravascular, and interstitial components induced by the measurable fibrotic and inflammatory response to bleomycin.