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PubMed2004

p21(Cip-1/SDI-1/WAF-1) expression via the mitogen-activated protein kinase signaling pathway in insulin-induced chondrogenic differentiation of ATDC5 cells.

The embryonal carcinoma-derived cell line, ATDC5, differentiates into chondrocytes in response to insulin or insulin-like growth factor-I stimulation. In this study, we investigated the roles of mitogen-activated protein (MAP) kinases in insulin-induced chondrogenic differentiation of ATDC5 cells. Insulin-induced accumulation of glycosaminoglycan and expression of chondrogenic differentiation markers, type II collagen, type X collagen, and aggrecan mRNA were inhibited by the MEK1/2 inhibitor (U0126) and the p38 MAP kinase inhibitor (SB203580). Conversely, the JNK inhibitor (SP600125) enhanced the synthesis of glycosaminoglycan and expression of chondrogenic differentiation markers. Insulin-induced phosphorylation of ERK1/2 and JNK but not that of p38 MAP kinase. We have previously clarified that the induction of the cyclin-dependent kinase inhibitor, p21(Cip-1/SDI-1/WAF-1), is essential for chondrogenic differentiation of ATDC5 cells. To assess the relationship between the induction of p21 and MAP kinase activity, we investigated the effect of these inhibitors on insulin-induced p21 expression in ATDC5 cells. Insulin-induced accumulation of p21 mRNA and protein was inhibited by the addition of U0126 and SB203580. In contrast, SP600125 enhanced it. Inhibitory effects of U0126 or stimulatory effects of SP600125 on insulin-induced chondrogenic differentiation were observed when these inhibitors exist in the early phase of differentiation, suggesting that MEK/ERK and JNK act on early phase differentiation. SB202580, however, is necessary not only for early phase but also for late phase differentiation, indicating that p38 MAP kinase stimulates differentiation by acting during the entire period of cultivation. These results for the first time demonstrate that up-regulation of p21 expression by ERK1/2 and p38 MAP kinase is required for chondrogenesis, and that JNK acts as a suppressor of chondrogenesis by down-regulating p21 expression.

Animals↗

PubMed1996

Phosphorylation of c-Fos at the C-terminus enhances its transforming activity.

c-Fos is phosphorylated by MAP kinase and the 90 kDa-ribosomal S6 kinase (RSK) in vitro at serines 362 and 374 (rat) which we demonstrate are major in vivo phosphorylation sites in early G1. We have constructed c-Fos mutants with these serines changed to aspartic acid residues (FosD) to mimic phosphorylation or to alanine residues (FosA) to prevent phosphorylation. Cells expressing FosD exhibited a more extensive transformed phenotype than those expressing either FosA or wild type c-Fos (FosWT). We also observed that FosA has a reduced half-life in comparison with FosD in G1. Furthermore, we observed enhanced AP-1 transactivation activity in cells expressing FosD. These results indicate that phosphorylation of c-Fos at its extreme carboxyterminus, possibly by MAP kinase and RSK, supports the proliferative response by increasing c-Fos stability and/or by increasing its transactivation activity. Under conditions in which the MAP kinase pathway is constitutively activated, c-Fos phosphorylation probably contributes to cellular transformation. The highly conserved nature of these phosphorylation sites in other c-fos family members suggests that these may also be targets of MAP kinase and RSK.

3T3 Cells↗

PubMed2005

Optimizing the evidence for linkage by permuting marker order.

We developed a new marker-reordering algorithm to find the best order of fine-mapping markers for multipoint linkage analysis. The algorithm searches for the best order of fine-mapping markers such that the sum of the squared differences in identity-by-descent distribution between neighboring markers is minimized. To test this algorithm, we examined its effect on the evidence for linkage in the simulated and the Collaborative Studies on Genetics of Alcoholism (COGA) data. We found enhanced evidence for linkage with the reordered map at the true location in the simulated data (p-value decreased from 1.16 x 10(-9) to 9.70 x 10(-10)). Analysis of the White population from the COGA data with the reordered map for alcohol dependence led to a significant change of the linkage signal (p = 0.0365 decreased to p = 0.0039) on chromosome 1 between marker D1S1592 and D1S1598. Our results suggest that reordering fine-mapping markers in candidate regions when the genetic map is uncertain can be a critical step when considering a dense map.

Alcoholism↗

PubMed2003

Myopic astigmatism and presbyopia trial.

PURPOSE: No prospective double-masked study has evaluated whether low astigmatism benefits or harms patients with presbyopia, whose intermediate and near vision might theoretically benefit from enhanced depth of focus provided by astigmatism. The purpose of the first Myopic Astigmatism and Presbyopia (MAP I) study was to determine whether low myopic astigmatism enhances or harms the visual acuity, stereopsis, or quality of life in patients with presbyopia. DESIGN: Prospective, randomized, double-masked, crossover design clinical trial. METHODS: Fifteen patients with presbyopia aged 45 to 68 years were recruited from an academic center population. These patients were given a baseline eye examination, including manifest refraction, Early Treatment of Diabetic Retinopathy Study (ETDRS) logarithm of minimal angle of resolution (logMAR) visual acuity at distance, intermediate, and near, accommodative amplitudes, and stereo vision. Each patient was then cycled in random order through three masked pairs of soft contact lenses. The power of each contact lens pair was calculated by the subtraction method to maintain a spherical equivalent of -0.5 diopters, while providing either no astigmatism (spherical arm, SPH), 1 diopter of with-the-rule (WTR) astigmatism, or 1 diopter of against-the-rule (ATR) astigmatism. Actual refractive errors produced were measured by masked examiner. Outcomes measured at the end of 1 week of usage of each contact lens arm were binocular (ETDRS) logMAR visual acuity at three distances (far [4 m], intermediate [1 m], and near [33cm]); near stereoacuity, using the quantitative Titmus Stereotest; and quality of life, measured using the Refractive Status and Vision Profile (RSVP), a standardized questionnaire. RESULTS: Visual acuity results across the three arms were similar. However, 1-m logMAR visual acuity was better for the spherical arm than either astigmatic arm (-0.06 SPH, +0.01 WTR, +0.02 ATR). Near (33 cm) and distance (4 m) acuities were similar across arms. Stereoacuity was better in ATR than WTR (50 vs 102 seconds, P =.01). Subjects preferred SPH slightly over the WTR astigmatic arm by the RSVP quality-of-life survey instrument (101 vs 104, P =.05). Other intergroup comparisons showed no difference in RSVP scores. CONCLUSIONS: This study has demonstrated that intermediate distance acuity and refractive quality of life are slightly better with spherical low myopic refractive error vs either astigmatic arm. Near and far distance acuity were unaffected by low myopic astigmatism compared with spherical low myopia. Near stereopsis was best in the ATR arms, but this did not produce better near visual acuity or RSVP quality of life.

Aged↗

PubMed2006

Selective serotonin reuptake inhibitors, fluoxetine and paroxetine, attenuate the expression of the established behavioral sensitization induced by methamphetamine.

To obtain an insight into the development of a new pharmacotherapy that prevents the treatment-resistant relapse of psychostimulant-induced psychosis and schizophrenia, we have investigated in the mouse the effects of selective serotonin reuptake inhibitors (SSRI), fluoxetine (FLX) and paroxetine (PRX), on the established sensitization induced by methamphetamine (MAP), a model of the relapse of these psychoses, because the modifications of the brain serotonergic transmission have been reported to antagonize the sensitization phenomenon. In agreement with previous reports, repeated MAP treatment (1.0 mg/kg a day, subcutaneously (s.c.)) for 10 days induced a long-lasting enhancement of the increasing effects of a challenge dose of MAP (0.24 mg/kg, s.c.) on motor activity on day 12 or 29 of withdrawal. The daily injection of FLX (10 mg/kg, s.c.) or PRX (8 mg/kg, s.c.) from 12 to 16 days of withdrawal of repeated MAP administration markedly attenuated the ability of the MAP pretreatment to augment the motor responses to the challenge dose of the stimulant 13 days after the SSRI injection. The repeated treatment with FLX or PRX alone failed to affect the motor stimulation following the challenge of saline and MAP 13 days later. These results suggest that the intermittent and repetitive elevation of serotonergic tone may inhibit the expression of the motor sensitization induced by pretreatment with MAP. It is proposed that clinically available serotonin reuptake inhibitors could be useful for preventing the recurrence of hallucinatory-paranoid state in drug-induced psychosis and schizophrenia.

Animals↗

PubMed1996

Stimulation of C2C12 myoblast growth by basic fibroblast growth factor and insulin-like growth factor 1 can occur via mitogen-activated protein kinase-dependent and -independent pathways.

It is now well-recognized that the mitogen-activated protein (MAP) kinase cascade facilitates signaling from an activated tyrosine kinase receptor to the nucleus. In fact, an increasing number of extracellular effectors have been reported to activate the MAP kinase cascade, with a significant number of cellular responses attributed to this activation. We set out to explore how two extracellular effectors, basic fibroblast growth factor (bFGF) and insulin-like growth factor 1 (IGF-1), which have both been reported to activate MAP kinase, generate quite distinct cellular responses in C2C12 myoblasts. We demonstrate here that bFGF, which is both a potent mitogen and inhibitor of myogenic differentiation, is a strong MAP kinase agonist. By contrast, IGF-1, which is equally mitogenic for C2C12 cells but ultimately enhances the differentiated phenotype, is a weak activator of the MAP kinase cascade. We further demonstrate that IGF-1 is a potent activator of both insulin receptor substrate IRS-1 tyrosyl phosphorylation and association of IRS-1 with activated phosphatidylinositol 3-kinase (PI 3-kinase). Finally, use of the specific MAP kinase kinase inhibitor, PD098059, and wortmannin, a PI 3-kinase inhibitor, suggests the existence of an IGF-1-induced, MAP kinase-independent signaling event which contributes to the mitogenic response of this factor, whereas bFGF-induced mitogenesis appears to strongly correlate with activation of the MAP kinase cascade.

Androstadienes↗

PubMed1995

Use of a 64 channel computerized cardiac mapping system in arrhythmia surgery.

A multipoint and computerized intraoperative mapping system has been known to be of value in improving the results of surgery for cardiac arrhythmia. It shows great potential as a new tool in the surgical intervention of the more common and lethal types of supraventricular tachyarrhythmias such as atrial flutter and atrial fibrillation. In addition, it also enhances the ability of the investigators to map and ablate the sometimes fleeting automatic atrial tachycardia. The authors developed a 64 channel computerized cardiac mapping system using a microcomputer (Macintosh IIx) and this has been used for basic research in cardiac electrophysiology as well as in arrhythmia surgery. In this system, bipolar electrograms are obtained from 64 different cardiac sites simultaneously at a sampling rate of 1 Ksample/sec and with a continuous and total data storage of up to 30 seconds. When the reference electrode is selected, delay time from the reference point is displayed on a two dimensional diagram of the heart. This system was used in one patient who underwent a surgical ablation of a ventricular tachycardia in whom we observed a ventricular activation sequence involving a variety of rhythms over several minutes. The system design permits easy expansion to a simultaneous sampling from 256 sites. This 64-channel mapping appeared to have the potential to be of great help in our understanding of cardiac arrhythmia as well as in its diagnosis and surgical treatment.

Arrhythmias, Cardiac↗

PubMed1997

Regulation of cell motility by mitogen-activated protein kinase.

Cell interaction with adhesive proteins or growth factors in the extracellular matrix initiates Ras/mitogen-activated protein (MAP) kinase signaling. Evidence is provided that MAP kinase (ERK1 and ERK2) influences the cells' motility machinery by phosphorylating and, thereby, enhancing myosin light chain kinase (MLCK) activity leading to phosphorylation of myosin light chains (MLC). Inhibition of MAP kinase activity causes decreased MLCK function, MLC phosphorylation, and cell migration on extracellular matrix proteins. In contrast, expression of mutationally active MAP kinase kinase causes activation of MAP kinase leading to phosphorylation of MLCK and MLC and enhanced cell migration. In vitro results support these findings since ERK-phosphorylated MLCK has an increased capacity to phosphorylate MLC and shows increased sensitivity to calmodulin. Thus, we define a signaling pathway directly downstream of MAP kinase, influencing cell migration on the extracellular matrix.

Animals↗

PubMed2026

Educational approaches to enhance genomics competencies among health sciences students: A scoping review with implications for nursing education.

INTRODUCTION: Genomics is increasingly recognized as essential for precision health, yet its integration into undergraduate nursing and other health sciences curricula remains limited. Persistent gaps in genomics literacy and confidence among students and professionals indicate that current educational approaches may not adequately prepare graduates for genomics-informed care and precision health. The aim of this review is to map educational approaches and methods used to enhance genomic competencies among undergraduate health sciences students and discuss implications for nursing education. METHODS: Scoping review, reported in accordance with PRISMA-ScR recommendations. Systematic search in CINAHL Ultimate, ERIC, and MEDLINE for studies published in English between January 2015 and December 2024 was undertaken. Data were charted using a standardized extraction form and synthesized descriptively and narratively, grouping interventions by educational approach, methods, strategies, techniques, and tools. RESULTS: Thirty-one studies were included, mostly from the United States, involving primarily medical and nursing students. Educational approaches centered on experiential and practice-based learning, simulation, case- and problem-based learning, flipped classrooms, collaborative or interprofessional learning, narrative and arts-based methods, and technology-enhanced strategies such as virtual labs, online modules, and digital storytelling. These approaches were associated with improvements in genomic knowledge, application to clinical scenarios, ethical awareness, engagement, and self-reported confidence, although outcomes were predominantly short-term. CONCLUSIONS: Genomics education for health sciences students is characterized by diverse, largely experiential and student-centered approaches. Integration into curricula remains fragmented and often focused on genetics rather than broader genomics and precision health. Nurse educators should prioritize integrated, authentic, and ethically informed genomics education, supported by educator development and digital technologies, including generative AI, to prepare graduates for precision nursing care.

Genomics↗

PubMed1989

Tissue-specific and hormonal regulation of angiotensinogen minigenes in transgenic mice.

Angiotensinogen is the precursor of the potent vasoactive peptide angiotensin II, and is therefore an important determinant of blood pressure and electrolyte homeostasis. In order to map the tissue-specific and inducible enhancer elements governing angiotensinogen gene expression in transgenic mice, we constructed minigenes containing either 0.75 kb or 4 kb or 5' flanking DNA from the BALB/c angiotensinogen gene. Sequences necessary and sufficient to mediate induction by glucocorticoids, oestrogen and bacterial endotoxin were contained on the minigene bearing 0.75 kb of DNA upstream of the capsite. This construct was also able to confer tissue specificity in the majority of organs producing angiotensinogen. In the testis and salivary gland, differences between the donor (BALB/c) and recipient (Swiss) strains were responsible for the apparently aberrant expression of the minigene constructs. The genetic lesion responsible for these expression polymorphisms has been characterized using recombinant inbred mice. An EcoRI restriction fragment length polymorphism which co-segregates with the angiotensinogen expression phenotypes into many inbred mouse strains is also described.

Angiotensinogen↗

PubMed1993

Magnetic resonance imaging of the mediastinum.

Magnetic resonance (MR) imaging is becoming a primary modality for evaluating the mediastinum. MR affords multiplanar imaging capabilities without exposing patients to ionizing radiation. The inherent contrast effect of different mediastinal tissues sharply delineates anatomic structures on MR images without contrast enhancement. Gradient-echo and phase-mapping techniques permit noninvasive qualitative and quantitative assessment of mediastinal blood flow. High soft tissue contrast and flow analysis capabilities make MR imaging a valuable modality for evaluating mediastinal vascular disorders. Various mediastinal tumors and their extent are best identified by the use of T1-weighted, T2-weighted, and gadolinium-enhanced images. Both primary and secondary chest wall lesions may be assessed with standard spin-echo MR images. Complex pleuroparenchymal lesions may be evaluated by means of a multiplanar approach and modified pulse sequences. This article addresses the technical parameters governing MR imaging of the mediastinum and describes MR characteristics of various pathologic conditions.

Humans↗

PubMed1997

An androgen response element in a far upstream enhancer region is essential for high, androgen-regulated activity of the prostate-specific antigen promoter.

Prostate-specific antigen (PSA) is expressed at a high level in the luminal epithelial cells of the prostate and is absent or expressed at very low levels in other tissues. PSA expression can be regulated by androgens. Previously, two functional androgen-response elements were identified in the proximal promoter of the PSA gene. To detect additional, more distal control elements, DNasel-hypersensitive sites (DHSs) upstream of the PSA gene were mapped in chromatin from the prostate-derived cell line LNCaP grown in the presence and absence of the synthetic androgen R1881. In a region 4.8 to 3.8 kb upstream of the transcription start site of the PSA gene, a cluster of three DHSs was detected. The middle DNAseI-hypersensitive site (DHSII, at approximately -4.2 kb) showed strong androgen responsiveness in LNCaP cells and was absent in chromatin from HeLa cells. Further analysis of the region encompassing DHSII provided evidence for the presence of a complex, androgen-responsive and cell-specific enhancer. In transient transfected LNCaP cells, PSA promoter constructs containing this upstream enhancer region showed approximately 3000-fold higher activity in the presence than in the absence of R1881. The core region of the enhancer could be mapped within a 440-bp fragment. The enhancer showed synergistic cooperation with the proximal PSA promoter and was found to be composed of at least three separate regulatory regions. In the center, a functionally active, high-affinity androgen receptor binding site (GGAACATATTGTATC) could be identified. Mutation of this element almost completely abolished PSA promoter activity. Transfection experiments in prostate and nonprostate cell lines showed largely LNCaP cell specificity of the upstream enhancer region, although some activity was found in the T47D mammary tumor cell line.

Androgens↗

PubMed2002

Motor map expansion following repeated cortical and limbic seizures is related to synaptic potentiation.

The effect of experimentally induced seizure activity on the functional reorganization of motor maps has not previously been investigated. Furthermore, while the functional reorganization of motor maps has been thought to involve increases in synaptic communication, there has yet to be a test of this hypothesis. Here we show that repeated seizure activity (kindling), that is accompanied by increased synaptic strength within adult rat motor cortex, results in a doubling of the caudal forelimb motor area. We measured neo-cortical evoked potentials in the right hemisphere prior to 25 days of electrical kindling of the medial frontal corpus callosum or amygdala and re-measured them either 1 or 21 days following the last kindling session. Then, using high resolution intracortical microstimulation (ICMS), the caudal forelimb area in the left hemisphere was mapped. This is the first report of any procedure causing a motor representation to double in size. Furthermore, this expansion was related to the enhanced area of a neocortical polysynaptic field potential and not the motor convulsions per se. Moreover, both the motor map and field potential enhancements were persistent in nature and could be driven from either cortical or limbic sites. The data have implications for human populations with epilepsy.

Animals↗

PubMed1995

1995 AUR Memorial Award. Gamma knife irradiation-induced changes in the normal rat brain studied with 1H magnetic resonance spectroscopy and imaging.

RATIONALE AND OBJECTIVES: The pathogenesis of brain injury following radiosurgery is poorly understood. To better elucidate the relationship between blood-brain barrier disruption and metabolic derangements, we used magnetic resonance (MR) imaging and 1H MR spectroscopy to detect early changes from focused single-fraction, high-dose irradiation injury in rat brains. METHODS: Using the Leksell gamma knife, we irradiated the frontoparietal cortex of 11 male Wistar rats with a single dose of 120 Gy. Four weeks later, we sequentially performed water-suppressed 1H MR spectroscopy and gadopentetate dimeglumine-enhanced T1-weighted MR imaging. Metabolic maps were created of n-acetylaspartate (NAA), creatine and choline (Cr/Cho), and lactate from the MR spectroscopy data set. Detection of irradiation injury among the tested modalities was assessed by receiver operating characteristic analysis and by quantitative signal intensity changes. Pathologic confirmation of irradiation damage was obtained in all rats. RESULTS: Gadopentetate dimeglumine-enhanced T1-weighted MR imaging was the only imaging modality that detected statistically significant signal intensity changes (p < .05). No reproducible changes in the metabolites of interest could be detected by 1H MR spectroscopy. CONCLUSION: In our animal model, blood-brain barrier disruption was a reproducible, integral finding of single-fraction, high-dose irradiation injury. No reproducible metabolic derangements of ischemia or necrosis were detected by 1H MR spectroscopy, possibly because of dose-latency effects or sensitivity issues.

Animals↗

PubMed1996

MRI mapping of microvascular permeability and tissue blood volume.

A quick and automated method for quantitative spatial mapping of tissue characteristics derived from contrast enhanced MR imaging by a macromolecular contrast medium (MMCM) was used in normal rats. Specifically, an established two compartment unidirectional flow kinetic model was automatically implemented on a pixel by pixel basis to calculate permeability surface area product (PS) and tissue fractional blood volume (BV) from MRI dynamic intensity data. The utility of PS and BV maps were evaluated in the normal rat abdomen where a range of fractional BV was found: from 100% in the vena cava to 1% in skeletal muscles, with intermediate values for liver and kidney. Tissue permeability depicted on the PS maps was generally low for normal tissues.

Animals↗

PubMedDate not supplied

Physiologic changes in breast magnetic resonance imaging during the menstrual cycle: perfusion imaging, signal enhancement, and influence of the T1 relaxation time of breast tissue.

This study was undertaken to determine the best time during the menstrual cycle to perform dynamic breast magnetic resonance imaging (MRI). The contralateral "normal" breast of 50 premenopausal women (mean age 40.4 +/- 6.4 years, range 30--52 years) were enrolled in a protocol designed to correlate an ipsilateral suspicious breast lesion with pathology. The contralateral breast in each patient was examined with palpation and mammography prior to MRI on a 1.5 T scanner using gradient echo and dynamic contrast-enhanced echo-planar without and following gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) injection. Pre-contrast T1 relaxation times were measured before calculating extraction flow product (EFP) maps using a multicompartmental model. T1, EFP, and enhancement were measured in the control breast on four slices centered around the nipple and recorded as a function of the phases of the menstrual cycle. Lesions or areas with focal enhancement were excluded. Analysis of variance and Fisher's tests were performed. The cyclic changes in T1 relaxation time were not significant (p>0.2). EFP and enhancement varied significantly during the cycle (p<0.003 and p<0.004, respectively), with low values during the first half of the cycle and high values during the second half. The lowest values of EFP and enhancement (5.5+/-2.9 ml/100 g/min and 26+/-17%) were observed during the proliferative phase (days 3--7), and the highest values (17+/-10.2 ml/100 g/min and 104+/-28%) were observed during the secretory phase (days 21-27) (p<0.0006 and p<0.0008, respectively). Dynamic breast MRI should be performed during first half of the menstrual cycle (days 3--14) in order to minimize interpretative difficulties related to the uptake of gadolinium in normal breast tissue due to hormonal fluctuations during the menstrual cycle.

Adult↗

PubMed1999

Walking through a maze alters the architecture of sleep.

Human and animal studies imply that sleep is a critical period for consolidation of recent memories. Whereas the majority of researchers focussed on the procedural learning, the present human study concerns how storing of spatial information and episodic memory are linked to sleep stages. Two city mazes, a simple and a complex one, were created by means of a computer program. Local aspects of these mazes appeared as street scenes on a TV-screen. Our subjects sat in front of the screen and manoeuvered through the maze by the help of a three-button PC mouse. Thus, each subject took a 'mental walk' through an imaginary city. The task was to find various end-points and to find the way back to the starting point. Subjects of two experimental groups 'walked' through either the simple or complex city maze for eight hours. Afterwards the subjects slept in our laboratory, where their sleep stages could be measured polygraphically. Subjects who had explored the simple maze showed considerable alteration in sleep architecture. They remained significantly longer in sleep Stage 2 than subjects who had explored the complex maze. Moreover, with successful orientation in the simple maze sleep stages occurred aperiodically, whereas walking through the complex maze was associated with sleep stages in accordance with ultradian cycles, as observed in a control group. Compared to subjects of the control group who had experienced neither maze, the subjects of both experimental groups had significantly enhanced EEG sleep spindle activities. Alteration in temporal architecture of sleep and selective prolongation of sleep Stage 2 following spatial orientation point to a functional linkage between cognitive mapping of space and sleep Stage 2 with enhanced EEG spindle activity.

Activity Cycles↗

PubMed2002

Temporal changes in reversible cerebral ischemia on perfusion- and diffusion-weighted magnetic resonance imaging: the value of relative cerebral blood volume maps.

Using a transorbital approach we induced the temporal occlusion and reperfusion model in 18 cats. A vascular clamp was placed on the main trunk of the left middle cerebral artery (MCA) for 1 h. Diffusion- and perfusion-weighted MR images were obtained at 1, 3, 6 and 24 h after the clip was released. The cats were killed 24 h after reperfusion, and triphenyl tetrazolium chloride (TTC) staining was performed. After the relative cerebral blood volume (rCBV), time to peak enhancement (TTP) and apparent diffusion coefficient (ADC) maps had been acquired, ROIs were drawn on (1) the area of the infarct produced, (2) the area of high signal intensity on initial diffusion-weighted magnetic resonance imaging (DWI) but normal on TTC staining, e.g., salvaged parenchyma. The ratios of these areas to the normal contralateral cortex were calculated and compared with those of the areas of the final infarct and the salvaged parenchyma. Areas of final infarct showed a temporal increase of rCBV on 3 and 6-h imaging and a final depletion on 24-h imaging. A persistent decrease of ADC value and delayed TTP were observed. Salvaged parenchyma also showed increased rCBV after reperfusion until the last imaging comparing it to the final area of infarct (P < 0.05, 24-h rCBV). The initial decrease in the ADC and delayed TTP normalized on 24-h imaging. In conclusion, rCBV of 24-h imaging was the reliable parameter to predict final infarct. A combination of serial changes on DWI and perfusion-weighted imaging (PWI) can predict ischemic penumbra and outcome.

Animals↗