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Results for “Enhancer mapping”

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PubMed1995

Effects of fentanyl on sympathetic activation associated with the administration of desflurane.

BACKGROUND: Activation of the sympathetic nervous system occurs when desflurane is inspired shortly after anesthetic induction and when the inspired concentration of desflurane is rapidly increased during steady-state periods of anesthesia. The purpose of this study was to determine the effectiveness and dose response of fentanyl pretreatment in attenuating the neurocirculatory responses to desflurane in healthy human volunteers. METHODS: After Institutional Research Review Board approval, three study groups were selected and, in random order, received either placebo (n = 10), a 2.5-micrograms.kg-1 intravenous bolus of fentanyl citrate followed by a continuous infusion of 1 microgram.kg-1.h-1 (n = 9), or a 5.0-micrograms.kg-1 intravenous bolus followed by an infusion of 2 micrograms.kg-1.h-1 (n = 11) before the administration of desflurane. Arterial (MAP) and central venous (CVP) pressures were measured directly, and heart rate (HR) was determined indirectly. Efferent muscle sympathetic nerve activity (SNA) was recorded from the peroneal nerve by microneurography. After neurocirculatory recordings at conscious unmedicated baseline and 12 min after fentanyl administration, anesthetic induction was carried out with 2.0 mg.kg-1 propofol and 0.2 mg.kg-1 vecuronium. Neurocirculatory measurements were repeated beginning 2 min after induction when desflurane was given via mask (semiclosed circle system, 61/min fresh gas flow, 100% O2) in three incremental 1-min steps (3.6%, 7.2%, and 11%). Intubation occurred 10 min after propofol administration. Twenty minutes after intubation, recordings were obtained during two steady-state periods during which end-tidal concentrations had achieved 5.4% (0.75 MAC) and 11% (1.5 MAC) desflurane for at least 10 min. Data also were obtained during the rapid increase in the inspired gas concentration from 5.4% to 11% ("transition"). RESULTS: Neurocirculatory variables did not differ between the three groups at conscious baseline, after fentanyl, and during steady-state periods of anesthesia. Propofol administration significantly reduced SNA and MAP. The MAP reduction was enhanced in the fentanyl-treated groups. After induction, the increases in SNA and MAP associated with the administration of desflurane by mask were not significantly reduced by fentanyl. The transition from 5.4% to 11% desflurane resulted in increases in SNA, HR, MAP, and fentanyl administration significantly attenuated the HR and MAP components. At the 11% steady-state measurement period, CVP was increased and MAP was decreased from conscious baseline, and these changes were not modified by fentanyl. CONCLUSIONS: The administration of desflurane was associated with increases in SNA, HR, MAP, and CVP. Maximum sympathetic activation and hemodynamic responses occurred 4-5 min after initiating desflurane during induction and 2-3 min after increasing the inspired concentration of desflurane during the "transition" period. Although fentanyl partially attenuated the hemodynamic component in a dose-dependent fashion during the "transition" period, it did not significantly diminish the response during induction.

Adult↗

PubMed2002

Divergent regulation by p44/p42 MAP kinase and p38 MAP kinase of bone morphogenetic protein-4-stimulated osteocalcin synthesis in osteoblasts.

In the present study, we investigated whether the mitogen-activated protein (MAP) kinase superfamily is involved in the bone morphogenetic protein (BMP)-4-stimulated synthesis of osteocalcin in osteoblast-like MC3T3-E1 cells. BMP-4 dose-dependently stimulated osteocalcin synthesis. BMP-4 markedly induced the phosphorylation of p44/p42 MAP kinase and p38 MAP kinase, while having little effect on SAPK (stress-activated protein kinase)/JNK (c-Jun N terminal kinase) phosphorylation. SB203580 and PD169316, specific inhibitors of p38 MAP kinase, significantly reduced the osteocalcin synthesis stimulated by BMP-4. In contrast, PD98059 and U0126, inhibitors of upstream kinase of p44/p42 MAP kinase, markedly enhanced the BMP-4-stimulated osteocalcin synthesis. The BMP-4-induced phosphorylation of p44/p42 MAP kinase was suppressed by PD98059, which did not, however, affect the BMP-4-induced phosphorylation of p38 MAP kinase. Taken together, our results strongly suggest that p38 MAP kinase takes part in BMP-4-stimulated osteocalcin synthesis as a positive regulator in osteoblasts, whereas p44/p42 MAP kinase acts as a negative regulator in the synthesis.

Bone Morphogenetic Protein 4↗

PubMed1997

Enhancement of EGF- and PMA-mediated MAP kinase activation in cells expressing the human papillomavirus type 16 E5 protein.

In this report we demonstrate that cells expressing the human papillomavirus type 16 E5 open reading frame (HPV16-E5) show a greatly enhanced transcription of the immediate early genes after EGF or PMA treatment compared to control cells. This enhancement is due to amplification of the signal transduction pathways in response to growth factors or phorbol esters. Upon short-time EGF treatment of the E5-expressing cells we observed an increase in the activation of EGF receptors, resulting in a stronger activation of MAP kinases ERK1/2 compared to control-transfected cells. We also observed that in E5-expressing cells, treatment with PMA results in an increase in membrane-associated PKC activity, and a superactivation of the ERK1/2 MAP kinases. This superactivation is PKC-dependent, since pretreatment of the cells with the PKC inhibitor Ro 31-8220 inhibits MAP kinase activation and early gene transcription almost completely. Furthermore, treatment with genistein strongly reduces the PMA-mediated superactivation of ERK1/2 kinases, demonstrating a PKC-mediated, tyrosine kinase-dependent pathway in the superinduction of MAP kinase activation. Thus, HPV16-E5 effects superactivation of MAP kinases over at least two different pathways, a PKC-mediated, and another, receptor tyrosine-kinase mediated, PKC-independent one.

3T3 Cells↗

PubMed2000

Mapping the growth of fungal hyphae: orthogonal cell wall expansion during tip growth and the role of turgor.

By computer-enhanced videomicroscopy, we mapped the trajectory of external and internal cell surface markers in growing fungal hyphae to determine the pattern of cell wall expansion during apical growth. Carbon particles (India ink) were chosen as external markers for tip expansion of Rhizoctonia solani hyphae. Irregularities in the growing apical walls of R. solani served as internal markers. Marker movement was traced in captured frames from the videotaped sequences. External and internal markers both followed orthogonal trajectories; i.e., they moved perpendicular to the cell surface regardless of their initial position in the hyphal apex. We found no evidence that the tip rotates during elongation. The discovery that the cell wall of a growing hypha expands orthogonally has major repercussions on two fronts: 1) It supports the long-held view that turgor pressure is the main force driving cell wall expansion. 2) It provides crucial information to complete the mathematical derivation of a three-dimensional model of hyphal morphogenesis based on the vesicle supply center concept. In three dimensions, the vesicle gradient generated by the vesicle supply center is insufficient to explain shape; it is also necessary to know the manner in which the existing surface is displaced during wall expansion.

Biophysical Phenomena↗

PubMed2004

A genetic linkage map of microsatellite, gene-specific and morphological markers in diploid Fragaria.

Diploid Fragaria provide a potential model for genomic studies in the Rosaceae. To develop a genetic linkage map of diploid Fragaria, we scored 78 markers (68 microsatellites, one sequence-characterised amplified region, six gene-specific markers and three morphological traits) in an interspecific F2 population of 94 plants generated from a cross of F.vesca f. semperflorens x F. nubicola. Co-segregation analysis arranged 76 markers into seven discrete linkage groups covering 448 cM, with linkage group sizes ranging from 100.3 cM to 22.9 cM. Marker coverage was generally good; however some clustering of markers was observed on six of the seven linkage groups. Segregation distortion was observed at a high proportion of loci (54%), which could reflect the interspecific nature of the progeny and, in some cases, the self-incompatibility of F. nubicola. Such distortion may also account for some of the marker clustering observed in the map. One of the morphological markers, pale-green leaf (pg) has not previously been mapped in Fragaria and was located to the mid-point of linkage group VI. The transferable nature of the markers used in this study means that the map will be ideal for use as a framework for additional marker incorporation aimed at enhancing and resolving map coverage of the diploid Fragaria genome. The map also provides a sound basis for linkage map transfer to the cultivated octoploid strawberry.

Base Sequence↗

PubMedDate not supplied

Simian virus 40 enhancer increases RNA polymerase density within the linked gene.

Enhancers are regulatory DNA elements, usually about 200 base pairs (bp) long, which are able to stimulate transcription of linked genes in eukaryotic cells. This activation can be exerted over large distances, and from a position 5' or 3' to the gene. Enhancers have been identified in viral genomes and cellular genes. Using a transient expression assay, we have analysed transcription of the rabbit beta-globin gene and the thymidine kinase gene from herpes simplex virus with and without a simian virus 40 (SV40) enhancer. S1 nuclease mapping shows a high level of specific transcripts when the genes are linked to the enhancer. To determine whether this increased number of transcripts is due to a higher transcription rate, or perhaps to a shift from nonspecific to specific initiation, we have performed run-on transcription assays with isolated nuclei. Our results, presented here, demonstrate that the SV40 enhancer increases the RNA polymerase density within the linked gene. Therefore, enhancers apparently increase the rate of transcription initiation without influencing the specificity of initiation.

Cell Nucleus↗

PubMed2002

Relationship between steroidogenic acute regulatory protein expression and progesterone production in hen granulosa cells during follicle development.

The present studies were conducted to address cellular mechanisms responsible for regulating steroidogenic acute regulatory protein (StAR) expression and progesterone synthesis at maturational stages corresponding to both the time of hen follicle selection, as well as before and after the LH surge in preovulatory follicle granulosa cells. A recently published report has established that mitogen-activated protein (MAP) kinase signaling induced by transforming growth factor alpha (TGFalpha) treatment blocks FSH-induced differentiation and StAR expression in cultured hen granulosa cells, whereas inhibitors of MAP kinase signaling enhance FSH-induced differentiation. The present in vitro studies demonstrate that in addition to MAP kinase signaling, activation of protein kinase C (PKC) blocks both FSH-induced StAR expression and the initiation of progesterone production in prehierarchal follicle granulosa cells, whereas the pharmacologic inhibitor of PKC, GF109203X, potentiates FSH-induced StAR expression and, as a consequence, the initiation of progesterone synthesis. Moreover, we demonstrate in granulosa cells collected from preovulatory follicles that although an acute increase in progesterone production in response to LH treatment requires rapid transcription and translation of StAR, the magnitude of progesterone production is rate-limited by one or more factors other than StAR (e.g., the P450 cholesterol side-chain enzyme). Finally, the rapid turnover of StAR protein, such as occurs following the withdrawal of LH, provides an additional mechanism for the tight regulation of progesterone production that occurs during the hen ovulatory cycle, and explains the rapid loss of steroidogenesis in the postovulatory follicle. In summary, data reported herein support the proposal that paracrine/autocrine factors (including but not necessarily limited to TGFalpha) prevent premature expression of StAR in prehierarchal follicle granulosa cells by more than one receptor-mediated signaling pathway. Furthermore, subsequent to follicle selection into the preovulatory hierarchy, StAR transcription and translation is necessary but not sufficient for the full potentiation of the preovulatory surge of serum progesterone.

Animals↗

PubMed1988

DNase I hypersensitivity is independent of endogenous topoisomerase II activity during chicken erythrocyte differentiation.

Endogenous topoisomerase II cleavage sites were mapped in the chicken beta A-globin gene of 12- to 14-day embryonic erythrocytes. A major topoisomerase II catalytic site was mapped to the 5' end of the globin gene which contained a nucleosome-free and DNase I-hypersensitive site and additional but minor sites were mapped to the second intron and 3' of the gene to a tissue-specific enhancer. Cleavage sites, mapped in situ by indirect end labeling, were aligned to single-base-pair resolution by comparison to a consensus sequence derived for vertebrate topoisomerase II catalytic sites. In contrast to embryonic erythrocytes, endogenous topoisomerase II cleavages were not detected in erythrocytes from peripheral blood of adult chickens; therefore, as the transcriptional activity of the beta A-globin gene declines during terminal differentiation of erythrocytes, the activity of topoisomerase II in situ declines as well, despite the fact that DNase I hypersensitivity persists. The results showed that DNase I-hypersensitive chromatin can be maintained in the absence of topoisomerase II activity and suggested that topoisomerase II acts at hypersensitive sites because of an inherent attraction to some preexisting combination of DNA sequence or chromatin structure associated with DNase I-hypersensitive regions.

Animals↗

PubMedDate not supplied

Automatic enhancement, animation, and segmentation of flow in peripheral arteries from MR phase-shift velocity mapping.

The authors describe a technique for automatic enhancement, segmentation, and analysis of flow from MR phase shift velocity mapping. This method uses a specific flow related enhancement process to extract and localize the flow field within the image, followed by global flow analysis. By animation on low cost equipment (personal computers), this method can provide various ways of visualizing flow in vivo and its variation in different structures and lesions. Our preliminary results using this method for analyzing flow data in the aortic bifurcation of healthy volunteers are encouraging.

Aorta, Abdominal↗

PubMed1998

Coronary vascular reactivity is improved by endothelin A receptor blockade in DOCA-salt hypertensive rats.

Endothelin-1 (ET-1) is thought to play an important role in the development of deoxycorticosterone acetate (DOCA)-salt hypertension. Because hypertension is associated with an increased incidence of coronary artery disease, this study was designed to determine if coronary vascular contraction to ET-1 is altered in DOCA-salt hypertensive rats and to determine the effect of chronic treatment of DOCA-salt rats with the selective ETA receptor antagonist A-127722. Male Sprague-Dawley rats were divided into four groups: DOCA, Placebo, DOCA + A-127722, and Placebo + A-127722. A-127722 was administered in drinking water at a concentration of 8 mg/100 ml. After 3 wk, mean arterial pressure (MAP) was significantly enhanced in DOCA-salt compared with Placebo rats. A-127722 significantly inhibited the increase in MAP. Contraction to ET-1 (10(-11) to 3 x 10(-8) M) was measured in isolated coronary and mesenteric small arteries (200-300 micron, intraluminal diameter) maintained at a constant intraluminal pressure of 40 mmHg and was significantly impaired in vessels from DOCA-salt compared with Placebo rats. Dose-dependent contractions to KCl were also inhibited in coronary, but only minimally impaired in mesenteric, arteries of DOCA-salt rats. Inhibition of nitric oxide synthase activity did not restore contraction to ET-1 in coronary small arteries. However contractions to ET-1 were enhanced in mesenteric small arteries. Chronic treatment with A-127722 significantly restored contraction to ET-1 in coronary, but not in mesenteric, arteries of DOCA-salt rats. Because ETA receptor blockade impairs the development of hypertension and improves coronary vascular reactivity, these data indicate that ET-1 plays an important role in coronary vascular dysfunction associated with DOCA-salt hypertension.

Animals↗

PubMed2006

Involvement of 5-HT receptors in the development and expression of methamphetamine-induced behavioral sensitization: 5-HT receptor channel and binding study.

Methamphetamine (MAP) is one of the most commonly abused drugs in Asia, and previous studies suggest that serotonin 3 receptors (5-HT(3)) are involved in MAP-induced locomotion and reward. However, little is known about the role of 5-HT(3) receptors in MAP-induced behavioral sensitization. Here, we measured the effects of MDL 72222, a 5-HT(3) antagonist, and SR 57227 A, a 5-HT(3) agonist, on the development and expression of MAP-induced behavioral sensitization, and alternations of 5-HT(3) receptor binding labeled with the 5-HT(3)-selective antagonist, [(3)H]GR65630, in mice. In addition, we investigated the effects of MAP on 5-HT(3A) receptor channel activity in Xenopus laevis oocytes expressing 5-HT(3A) receptors. We found that MDL 72222 attenuated both the development and expression of behavioral sensitization to MAP (1.0 mg/kg, i.p.), and that this attenuating effect of MDL 72222 was reversed by pre-treatment with SR 57227 A. In oocytes expressing 5-HT(3A) receptor, MAP exhibited a dual modulation of 5-HT(3A) receptor channel activity, i.e. pre-treatment with a low dose of MAP (0.1 microm) enhanced 5-HT-induced inward peak current (I(5-HT)) but a high dose of MAP (100 microm) inhibited I(5-HT). The acute administration of MDL 72222 with MAP decreased [(3)H]GR65630 binding versus MAP alone in the mouse striatum. Our results suggest that MDL 72222 attenuates MAP-induced behavioral sensitization via 5-HT(3) receptors in the caudate putamen, and that 5-HT(3) receptor antagonists like MDL 72222 have potential as novel anti-psychotic agents for the treatment of MAP dependence and psychosis.

Algorithms↗

PubMed2000

Genomics meets genetics: towards a mutant map of the mouse.

Phenotype-driven mutagenesis approaches in the mouse will deliver a vastly expanded mouse mutant resource and can be expected to lead to the identification of novel genes and pathways, enabling the emergence of new insights into mammalian gene function. In order for this goal to be realized, developments in genomics need to be harnessed to progress in mouse mutagenesis. We need firstly to generate a mutant map of the mouse, devising and employing rapid methods for the genetic mapping of the growing mouse mutant resource. Secondly, we need to be able to rapidly identify and assess candidate genes in the vicinity of the mapped mutations. Developments in mapping and genotyping technology are described that will potentially speed the construction of a rich mutant map of the mouse. In addition, the benefits of comparative sequencing of the human and mouse genomes are reviewed. The availability of both human and mouse genome sequences will underpin the evolution of a comprehensive and well annotated mammalian gene map that will significantly enhance our ability to move rapidly from mapped mutation to the identification of the underlying gene.

Animals↗

PubMed1999

Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region.

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 microgram/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 microliter/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 +/- 1 vs. 97 +/- 3 and 121 +/- 3 vs. 103 +/- 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.

Animals↗

PubMed1992

Brain ouabain and central effects of dietary sodium in spontaneously hypertensive rats.

High sodium intake (HNa) increases brain ouabainlike activity (OLA) in rats. In spontaneously hypertensive rats (SHR), HNa exaggerates development of hypertension and pressor and sympathoexcitatory responses to stress. To investigate whether dietary sodium-induced changes in brain OLA play a functional role, responses of mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) to intracerebroventricular ouabain and to mental stress and intracerebroventricular alpha 2-adrenoceptor agonist guanabenz alone or preceded by intracerebroventricular ouabain were recorded in conscious SHR and Wistar-Kyoto (WKY) rats maintained from 4 to 8 weeks of age on different sodium diets: 1) low sodium intake (LNa, 17 mumol), 2) normal sodium intake (NNa, 101 mumol), and 3) HNa (1,370 mumol). SHR on NNa showed significantly higher MAP and RSNA compared with WKY rats on NNa. HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats. Intracerebroventricular ouabain induced dose-dependent increases in MAP, RSNA, and HR. In both SHR and WKY rats, LNa significantly enhanced these responses. In contrast, HNa significantly attenuated these responses only in SHR. Air stress increased and intracerebroventricular guanabenz decreased MAP, HR, and RSNA. The magnitudes of increases and decreases were significantly larger in SHR than in WKY rats. In WKY rats, dietary sodium did not change these responses. In contrast, in SHR, HNa significantly enhanced MAP, HR, and RSNA responses to air stress or intracerebroventricular guanabenz.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Activation of p44/p42 mitogen-activated protein kinase limits triiodothyronine-stimulated alkaline phosphatase activity in osteoblasts.

It has been shown that thyroid hormone stimulates the activity of alkaline phosphatase, a marker of mature osteoblast phenotype, in osteoblasts. In the present study, we investigated whether p44/p42 mitogen-activated protein (MAP) kinase is involved in the thyroid hormone-stimulated alkaline phosphatase activity in osteoblast-like MC3T3-E1 cells. Triiodothyronine (T(3)) markedly induced the phosphorylation of p44/p42 MAP kinase. PD98059 and U0126, inhibitors of the upstream kinase that activates p44/p42 MAP kinase, significantly enhanced the T(3)-induced alkaline phosphatase activity in a dose-dependent manner. The phosphorylation of p44/p42 MAP kinase induced by T(3) was reduced by U0126. These results strongly suggest that p44/p42 MAP kinase takes part in the thyroid hormone-stimulated alkaline phosphatase activity in osteoblasts and that p44/p42 MAP kinase plays an inhibitory role in the thyroid hormone-effect.

3T3 Cells↗

PubMed2000

Preconditioning enhanced glucose uptake is mediated by p38 MAP kinase not by phosphatidylinositol 3-kinase.

Ischemia is reported to stimulate glucose uptake, but the signaling pathways involved are poorly understood. Modulation of glucose transport could be important for the cardioprotective effects of brief intermittent periods of ischemia and reperfusion, termed ischemic preconditioning. Previous work indicates that preconditioning reduces production of acid and lactate during subsequent sustained ischemia, consistent with decreased glucose utilization. However, there are also data that preconditioning enhances glucose uptake. The present study examines whether preconditioning alters glucose transport and whether this is mediated by either phosphatidylinositol 3-kinase (PI3K) or p38 MAP kinase. Langendorff-perfused rat hearts were preconditioned with 4 cycles of 5 min of ischemia and 5 min of reperfusion, with glucose as substrate. During the last reflow, glucose was replaced with 5 mM acetate and 5 mM 2-deoxyglucose (2DG), and hexose transport was measured from the rate of production of 2-deoxyglucose 6-phosphate (2DG6P), using (31)P nuclear magnetic resonance. Preconditioning stimulated 2DG uptake; after 15 min of perfusion with 2DG, 2DG6P levels were 165% of initial ATP in preconditioned hearts compared with 96% in control hearts (p < 0.05). Wortmannin, an inhibitor of PI3K, did not block the preconditioning induced stimulation of 2DG6P production, but perfusion with SB202190, an inhibitor of p38 MAP kinase, did attenuate 2DG6P accumulation (111% of initial ATP, p < 0. 05 compared with preconditioned hearts). SB202190 had no effect on 2DG6P accumulation in nonpreconditioned hearts. Preconditioning stimulation of translocation of GLUT4 to the plasma membrane was not inhibited by wortmannin. The data demonstrate that ischemic preconditioning increases hexose transport and that this is mediated by p38 MAP kinase and is PI3K-independent.

Adenosine Triphosphate↗

PubMed2006

Magnetic resonance-guided focused ultrasound surgery using an enhanced sonication technique in a pig muscle model.

THE PURPOSE OF THIS STUDY: To evaluate the safety and efficacy of an enhanced magnetic resonance-guided focused ultrasound (MRgFUS) emission protocol that results in more extensive treatment by increasing the volume of each focal ablation using the same energy. MATERIALS AND METHODS: Six pigs were treated with an MRgFUS system combined with real-time MR, for imaging and temperature mapping, with 102 "enhanced" and 97 "regular" focal ablations performed on both buttock muscles. Real-time imaging, temperature mapping, and acoustic reflected spectrum data enabled immediate evaluation of the results. MR contrast-enhanced images and pathology examinations were used for confirmation. RESULTS: The location of the ablated volume by "enhanced" sonication is predictable, with a maximum possible shift of 6 mm toward, and 3 mm away, from the transducer. The ablated volume after enhanced sonication was, on average, 1.8 times larger than after a regular sonication of the same energy. Pathology results showed the same thermally induced damage patterns in the enhanced sonications and the regular sonications. CONCLUSION: Accelerated MRgFUS with enhanced sonication is a safe, controllable, and more effective tissue ablative modality than standard sonication. This new technology may significantly reduce the length of tumor ablation procedures. (Isn't the new technology you're talking about MRgFUS? If so, you don't need to repeat it at the end of this sentence.).

Animals↗

PubMed2001

Validation of diffusion tensor magnetic resonance axonal fiber imaging with registered manganese-enhanced optic tracts.

Noninvasive mapping of white matter tracts using diffusion tensor magnetic resonance imaging (DTMRI) is potentially useful in revealing anatomical connectivity in the human brain. However, a gold standard for validating DTMRI in defining axonal fiber orientation is still lacking. This study presents the first validation of the principal eigenvector of the diffusion tensor in defining axonal fiber orientation by superimposing DTMRI with manganese-enhanced MRI of optic tracts. A rat model was developed in which optic tracts were enhanced by manganese ions. Manganese ion (Mn(2+)) is a potent T1-shortening agent and can be uptaken and transported actively along the axon. Based on this property, we obtained enhanced optic tracts with a T1-weighted spin-echo sequence 10 h after intravitreal injection of Mn(2+). The images were compared with DTMRI acquired with exact spatial registration. Deviation angles between tangential vectors of the enhanced tracts and the principal eigenvectors of the diffusion tensor were then computed pixel by pixel. We found that under signal-to-noise (SNR) of 30, the variance of deviation angles was (13.27 degrees). In addition, the dependence of this variance on SNR obeys stochastic behavior if SNR is greater than 10. Based on this relation, we estimated that an rms deviation of less than 10 degrees could be achieved with DTMRI when SNR is 40 or greater. In conclusion, our method bypasses technical difficulties in conventional histological approach and provides an in vivo gold standard for validating DTMRI in mapping white matter tracts.

Animals↗