Diffusion tensor magnetic resonance imaging of prostate cancer.

PURPOSE: To explore the feasibility of 3T magnetic resonance (MR) diffusion tensor imaging (DTI) and fiber tracking (FT) in patients with prostate cancer. MATERIALS AND METHODS: Thirty consecutive patients (mean age, 62.5 years) with biopsy proven prostate cancer underwent 3T-MR imaging (MRI) and DTI using a 6-channel external phased-array coil before radical prostatectomy. Regions of interest of 14 pixels were defined in tumors and nonaffected areas in the peripheral zone (PZ) and central gland (CG), according to histopatology after radical prostatectomy. Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) values were determined. Differences in mean ADC and FA values among prostate cancer, normal PZ and CG were compared by 2-sided Student t test. The predominant diffusion direction of the prostate anisotropy was color coded on a directionally encoded color (DEC) map. A 3D reconstruction of fiber tract orientations of the whole prostate was determined using the continuous tracking method. The overall image quality for tumor localization and local staging was assessed in retrospective matching with whole-mount section histopathology images. Nodules detected at MRI were classified as matched lesions if tumor presence and extension were evidenced at histopathology. RESULTS: For all the patients, the DTI sequence images were suitable for the evaluation of the zonal anatomy of the prostate gland and the tumor localization. Quantitative evaluation of the regions of interest (ROIs) showed a mean ADC value significantly lower in the peripheral neoplastic area (1.06 +/- 0.37 x 10(-3) mm2/s) than in the normal peripheral portion (1.95 +/- 0.38 x 10(-3) mm2/s) (P < 0.05). The mean FA values calculated in the normal peripheral (0.47 +/- 0.04) and central area (0.41 +/- 0.08) were very similar (P > 0.05). The mean FA values in the neoplastic lesion (0.27 +/- 0.05) were significantly lower (P < 0.05) than in the normal peripheral area and in the normal central and adenomyomatous area. DEC map showed a top-bottom type preferential direction in the peripheral but not in the central area, with the tumor lesions reducing the diffusion coding direction represented as color zones tending toward gray. Tractographic analysis permitted good delineation of the prostate anatomy (capsule outline, peripheral and central area borders) and neoplastic lesion extension and capsule infiltration compared with histopathology. CONCLUSIONS: Three Tesla DTI of the prostate gland is feasible and has the potential for providing improved diagnostic information.

The "Safari" technique to perform difficult subintimal infragenicular vessels.

The purpose of this study was to describe the efficacy of planned combined subintimal arterial flossing with antegrade-retrograde intervention (SAFARI) to obtain the precise recanalization of the patent portion of a distal runoff vessel in critical limb ischemia (CLI) patients presenting long occlusions involving the popliteal trifurcation. Four patients at risk of limb loss due to long occlusions involving the leg vessel tree and not suitable for a surgical bypass were treated by the subintimal antegrade and retrograde (posterior tibial or anterior tibial artery) approach. The patent portion of the runoff vessel was previously assessed by magnetic resonance angiography (MRA) and directly punctured under Doppler ultrasound (US) guidance. A subintimal channel rendezvous was performed to allow snaring of the guidewires. Subsequently, a balloon dilatation was performed without stent deployment. All patients were successfully recanalized and had complete healing of the limb lesions. At the 12-month follow-up all patients showed clinical improvement with no major complications related to the procedure. This combined antegrade and retrograde subintimal approach is currently an excellent endovascular option in patients with long occlusions extending onto the leg vessels trifurcation and at risk of limb loss.

Carotid artery stenting with filter protection in high-risk patients showing severe electroencephalographic alterations during carotid endarterectomy.

PURPOSE: To describe the results and efficacy of stent treatment in patients with carotid stenosis who had aborted carotid endarterectomy procedures due to the appearance of severe electroencephalographic (EEG) alterations. METHODS: A retrospective study was conducted of 18 patients (11 men; mean age 72 years, range 62-84) with symptomatic high-grade carotid artery stenoses (> or = 70%) who experienced severe EEG alterations during carotid endarterectomy, causing the procedure to be aborted. Twelve patients had shown no hemodynamic alterations during preoperative transcranial Doppler evaluation after external compression of the common carotid artery; the remaining 6 could not be evaluated. The patients were referred for carotid artery stenting (CAS); 7 had contralateral internal carotid artery stenosis and 5 had contralateral occlusion. Endovascular intervention was carried out using standard techniques under filter protection. Follow-up was scheduled at 3, 6, and 12 months. RESULTS: All patients were successfully treated without immediate complications. The EEG did not display any significant alterations during the endovascular procedure. Mean follow-up was 43 months. Magnetic resonance imaging at 6 months showed no signs of cerebral ischemia. Color Doppler ultrasound imaging documented normal stent patency in all patients. CONCLUSION: Patients with symptomatic severe carotid stenosis (> or = 70%) who are considered at risk due to the appearance of severe EEG alterations during surgical treatment may benefit from CAS with respect to both major and minor complications. Larger studies are needed to confirm these findings.

Management of biliary neoplastic obstruction with two different metallic stents implanted in one session.

The efficacy of the "one-step" technique using two different metallic stents (Wallstent and Ultraflex) and associated rate of complications was studied in 87 patients with jaundice secondary to malignant biliary obstruction, with bilirubin level less than 15 mg/dl and Bismuth type 1 or 2 strictures. The study group, composed of 40 men and 47 women with a mean age of 59.4 years (range 37-81 years), was treated with a "one-step" percutaneous transhepatic implantation of self-expanding stents. The cause of the obstruction was pancreatic carcinoma in 38 patients (44%), lymph node metastasis in 20 patients (23%), gallbladder carcinoma in 13 patients (15%), cholangiocarcinoma in 12 patients (14%) and ampullary carcinoma in four patients (5%). A significant reduction in jaundice was obtained in all but one patient, with a drop of total serum bilirubin level from a mean of 13.7 mg/dl to 4.3 mg/dl within the first 4 days. The mean postprocedural hospitalization period was 5.4 days in the Wallstent group and 6.4 days in the Ultraflex group. Mean survival rate was 7.8 months (Wallstent group) and 7.1 months (Ultraflex group). The use of both stents did not reveal any significant difference in parameters tested. The implantation of these self-expandable stents in one session, in selected patients, is clinically effective, devoid of important complications and cost-effective due to the reduction in hospitalization.

Downregulation of COX-2 and JNK expression after induction of ischemic tolerance in the gerbil brain.

The response of the inducible isoform of the prostaglandin H2 synthase (COX-2) and the c-Jun N-terminal kinase (JNK) in post-ischemic neuronal damage was assessed in a model of ischemic tolerance in Mongolian Gerbils. After a single 6-min bilateral carotid occlusion, histological damage was evident in the CA1 region of hippocampus, correlated with a high expression of JNK and COX-2 mRNA. However, in the group of animals with a 2-min ischemia and the tolerance group, in which a 2-min bilateral carotid occlusion was followed 3 days later by a 6-min ischemia, no hippocampal or cortical damage was detected. Accordingly, the JNK and COX-2 mRNA levels remained unaffected. We suggest that the level of JNK and COX-2 expression may determine the outcome as either post-ischemic cell death or tolerance.

Evaluation of anterior pituitary gland volume in childhood using three-dimensional MRI.

BACKGROUND: Three-dimensional MRI (3D-MRI) is a reliable tool for the evaluation of anatomical volumes. Volumetric measurement of the normal anterior pituitary gland in childhood has been performed in the past by 2D-MRI calculations, but has inherent inaccuracies. OBJECTIVE: To obtain accurate normal anterior pituitary gland volume in childhood using 3D-MRI coronal sections. MATERIALS AND METHODS: The anterior pituitary gland was measured using coronal T1-weighted 3D-gradient-echo sequences (section thickness 0.75 mm). The study group was composed of 95 prepubertal children (age range 2 months-10 years) with clinically normal pituitary function and no pituitary or brain abnormalities. RESULTS: A measurement error of 0.2-0.4% was assessed by using a phantom study. Volumetric evaluation of the anterior pituitary gland showed progressive growth of the gland from a mean 131+/-24 mm(3) at 2-12 months, to 249+/-25 mm(3) at 1-4 years and 271+/-29 mm(3) at 5-10 years. CONCLUSIONS: These data may be useful for paediatricians in the evaluation of patients with neuroendocrine diseases, in particular growth hormone deficiency.

Prostaglandins and other lipid mediators in Alzheimer's disease.

In the central nervous system (CNS), prostaglandin (PG) and other bioactive lipids regulate vital aspects of neural membrane biology, including protein-lipid interactions, trans-membrane and trans-synaptic signaling. However, a series of highly reactive PGs, free fatty acids, lysophospolipids, eicosanoids, platelet-activating factor, and reactive oxygen species (ROS), all generated by enhanced phospholipase A2 (PLA2) activity and arachidonic acid (AA) release, participate in cellular injury, particularly in neurodegeneration. PLA2 activation and PG production are among the earliest initiating events in triggering brain-damage pathways, which can lead to long-term neurologic deficits. Altered membrane-associated PLA2 activities have been correlated with several forms of acute and chronic brain injury, including cerebral trauma, ischemic damage, induced seizures in the brain and epilepsy, schizophrenia, and in particular, Alzheimer's disease (AD). Biochemical mechanisms of PLA2 overactivation and its pathophysiological consequences on CNS structure and function have been extensively studied using animal models and brain cells in culture triggered with PLA2 inducers, PGs, cytokines, and related lipid mediators. Moreover, the expression of both COX-2 and PLA2 appears to be strongly activated during Alzheimer's disease (AD), indicating the importance of inflammatory gene pathways as a response to brain injury. This review addresses some current ideas concerning how brain PLA2 and brain PGs are early and key players in acute neural trauma and in brain-cell damage associated with chronic neurodegenerative diseases such as AD.

Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: transcription and neurotrophic factor down-regulation and up-regulation of apoptotic and pro-inflammatory signaling.

Alterations in transcription, RNA editing, translation, protein processing, and clearance are a consistent feature of Alzheimer's disease (AD) brain. To extend our initial study (Alzheimer Reports [2000] 3:161-167), RNA samples isolated from control and AD hippocampal cornu ammonis 1 (CA1) were analyzed for 12633 gene and expressed sequence tag (EST) expression levels using DNA microarrays (HG-U95Av2 Genechips; Affymetrix, Santa Clara, CA). Hippocampal CA1 tissues were carefully selected from several hundred potential specimens obtained from domestic and international brain banks. To minimize the effects of individual differences in gene expression, RNA of high spectral quality (A(260/280) > or= 1.9) was pooled from CA1 of six control or six AD subjects. Results were compared as a group; individual gene expression patterns for the most-changed RNA message levels were also profiled. There were no significant differences in age, postmortem interval (mean < or = 2.1 hr) nor tissue pH (range 6.6-6.9) between the two brain groups. AD tissues were derived from subjects clinically classified as CDR 2-3 (CERAD/NIA). Expression data were analyzed using GeneSpring (Silicon Genetics, Redwood City, CA) and Microarray Data Mining Tool (Affymetrix) software. Compared to controls and 354 background/alignment markers, AD brain showed a generalized depression in brain gene transcription, including decreases in RNA encoding transcription factors (TFs), neurotrophic factors, signaling elements involved in synaptic plasticity such as synaptophysin, metallothionein III, and metal regulatory factor-1. Three- or morefold increases in RNAs encoding DAXX, cPLA(2), CDP5, NF-kappaBp52/p100, FAS, betaAPP, DPP1, NFIL6, IL precursor, B94, HB15, COX-2, and CEX-1 signals were strikingly apparent. These data support the hypothesis of widespread transcriptional alterations, misregulation of RNAs involved in metal ion homeostasis, TF signaling deficits, decreases in neurotrophic support and activated apoptotic and neuroinflammatory signaling in moderately affected AD hippocampal CA1.