The physical template (climate and topography) is commonly considered a principal factor in affecting vegetation structure and dynamics (Stephenson, 1990 and Urban et al., 2000). Human influences play a major role, however, in shaping the structure of forest stands and landscapes even in remote mountain areas of the world. Environmental fragility and seasonality of human activities, such as tourism, make mountain areas in developing regions particularly vulnerable to human-induced impacts (e.g. soil and vegetation trampling, disturbance to native wildlife, waste dumping) (Brohman, 1996). Tourism in mountain areas has increased in the last decades (Price, 1992) and is becoming

a critical environmental issue in many developing countries (Geneletti and Dawa, 2009). This is particularly evident in Nepal, where increased pressures of tourism-related activities on Etoposide price forest resources and the biodiversity of alpine shrub Ribociclib research buy vegetation have already been documented (Stevens, 2003). Sagarmatha National Park and its Buffer Zone (SNPBZ), a World Heritage Site inhabited by the Sherpa ethnic group and located in the Khumbu valley (Stevens, 2003), provides an example. The Himalayan region, which also includes the Sagarmatha (Mt.

Everest), has been identified as a globally important area for biodiversity (Olson et al., 2001) and is one of the world’s 34 biodiversity hotspots (Courchamp, 2013). Over the past 50 years, the Sagarmatha region has become a premier international mountaineering and trekking destination.

Related activities have caused adverse impacts on regional forests and alpine vegetation (Bjønness, 1980 and Stevens, 2003), with over exploitation of alpine shrubs and woody vegetation, overgrazing, accelerated slope erosion, and uncontrolled lodge building (Byers, 2005). Large areas surrounding the main permanent settlements in the region are extensively deforested, with Pinus wallichiana plantations partly replacing natural forests ( Buffa et al., 1998). Despite the importance of the Sagarmatha region, few studies have examined sustainable management and environmental conservation of its fragile ecosystems, where ecological and socio-economic issues are strongly linked (Byers, 2005). The lack of knowledge about forest Arachidonate 15-lipoxygenase structure and composition, as well as human impact on the ecosystems, has frequently limited the implementation of sustainable management plans (MFSC, 2007 and Rijal and Meilby, 2012). This study gathered quantitative data on forest resources and assessed the influences of human activities at Sagarmatha National Park (SNP) and its Buffer Zone (BZ). Using a multi-scale approach, we analyzed relationships among ecological, historical, topographic and anthropogenic variables to reveal the effects of human pressures on forest structure and composition.

It is interesting to note that the length of follow-up trended toward significance with close/positive-margin find more patients having longer follow-up than negative-margin patients (63.1 vs. 58.5 months, p = 0.06). This may represent surgeons increasingly attempting to achieve wider surgical margins in patients selected for APBI or a change in patient selection. Despite

these limitations, this analysis represents the largest collection of close/positive-margin APBI patients evaluated to date and supports the recommendation to obtain margins of 2 mm or greater before the adjuvant application of APBI. Good clinical outcomes were seen in patients undergoing APBI regardless of margin status. However, nonsignificant increases in the rates of IBTR were noted in patients with close or positive margins similar to

what is observed with WBI. Statistically significant increases in IBTR were noted for DCIS patients with close margins. Further prospective studies are required to validate these results and define the appropriate margin status for patients undergoing APBI. “
“Penile carcinoma accounts for 0.4–0.6% of all malignant neoplasms among men in Europe [1] and [2]. Its incidence may reach 20% in some Asian, African, and South American countries. Penile cancer is a disease of elderly men INCB018424 in Europe and North America, with a peak incidence in the sixth decade of life (3), although it may affect a younger age group

in developing countries. Most tumors of the penis are squamous cell carcinomas and occur most commonly on the glans, prepuce, and the coronal sulcus. For small lesions, treatment enabling the penis body to be preserved, notably penis brachytherapy (PB) (4), is recommended to improve the quality of life. Surprisingly, sexuality, which is nevertheless an important component of the quality of life in men with cancer, has not been well studied after conservative treatment of penile cancer. By analyzing a previous series of 51 patients treated between 1971 and 1989, we obtained information about the Thalidomide persistence of sexuality and penile erections of patients (5), but we did not have access to information on the impact of PB on all sexual functions and sexual behavior. To answer these questions, we established a database in the Catalan and Occitan Oncology Group, which includes two cancer centers each in France and Spain. We analyzed the oncologic outcome of penile cancer, and conducted a survey by questionnaire on the sexual functions and behavior after PB treatment, in the two French centers.

The chemiluminescent signal detected with a cooled CCD camera (Pierce, USA) was analyzed with ArrayVision 8.0 software (Imaging Research, USA). The sensitivity limit for each molecule was: CCL1 (0.8 pg/mL), CCL2 (0.8 pg/mL), CCL3 (3.1 pg/mL), CCL4 (0.8 pg/mL), CCL5 (0.4 pg/mL), CCL11 (0.5 pg/mL), CCL17 (0.4 pg/mL), CCL22 (0.2 pg/mL) and CXCL8 (0.2 pg/mL)

as provided by the manufacturer. For LMD-samples, all values below the limit of detection were assigned with the corresponding limit value. We strictly followed the manufacturer’s instructions and conducted selleck chemicals the assay in a blinded manner. LMD and plasma samples (with exception of temporal profiles) were assayed twice and the mean value of both measurements was given. For LMD-cell TSA HDAC clinical trial samples the resulting

chemokine protein concentration was finally corrected by the total protein content and values are given as pg/mg. Plasma results were expressed as pg/mL. Whole analysis was performed with SPSS 15.0 software (SPSS Inc., USA). Shapiro–Wilk test was used to define normally distributed variables (p > 0.05), due to small sample sizes. Normal distribution was analyzed by Students’ t test or ANOVA and mean and SD values were given. Different time points of temporal profiles were compared by ANOVA of repeated measures and paired-t test, while correlations with other continuous variables Interleukin-2 receptor were assessed by Pearson test. Non-normal distribution was assessed by Mann–Whitney U or Kruskal–Wallis

tests and median and interquartile range (IQR) were reported. We compared temporal profiles by Friedman and Wilcoxon tests, and analyzed correlations by Spearman test. Pearson chi-squared test was used to compare categorical variables. In all cases, a p-value <0.05 was considered statistically significant at a 95% confidence level. For sample size and statistical power calculation we compared medians by using Ene 3.0 free software (GlaxoSmithKline S.A., Spain; http://sct.uab.cat/estadistica/es). Of the nine chemokines assayed, CCL3, CCL4 and CCL17 were not detected in LMD-cell samples. Among the remaining six chemokines, CCL1 and CCL2 were found at higher levels in neurons than in blood vessels (p = 0.021 in both cases) only in healthy contralateral area. Interestingly, CCL5 and CCL22 were decreased within the vessels and neurons, respectively, when the contralateral region of the brain was compared to the infarcted tissue (both cases with a p = 0.043) ( Fig. 1). All the nine chemokines were detected in plasma samples of ischemic stroke patients and, as shown in Supplementary Table 2, no differences regarding demographic and clinical data were found between both studied cohorts.

3 and 1.0 g) [40], while 8 week-old growing mice exhibited a positive response in trabecular and cortical bone [38] and [39]. Investigations of WBV as a treatment for osteoporosis have shown

a positive impact on ovariectomized rats with greatest increase in bone mass at high frequencies [34], [41] and [43] while other investigation reported only an impact on cortical bone NLG919 concentration [42] or no substantial impact [45]. These variable results suggest a more complex involvement of the hormonal system in the mechano-sensitivity of bone to WBV. Interestingly, a positive osteogenic response to “limb vibration” in the absence of weight-bearing has been observed, suggesting an additional mechano-transduction pathway than pure CH5424802 molecular weight bone strain [9] and [46]. Previous WBV studies on both patients and

animals indicate that vibration is most effective in young growing bone and low density bone. Therefore WBV treatment may offer a promising route to non-invasively stimulate bone formation in OI children. The objectives of the present study were to investigate the effects of WBV on the cortical and trabecular bone formation in growing mice suffering a severe form of osteogenesis imperfecta (oim mice). All animal experiments followed the British Home office and institutional guidance (project license 70/6852). 24 Homozygous wild type (B6C3Fe-a/a-+/+) and 24 homozygous oim (B6C3Fe-a/a-oim/oim) female mice were bred. Due to a procollagen α2 gene ZD1839 in vivo recessive mutation, homozygous oim mice produce abnormal homotrimeric collagen type I (Col1-(α1)3) which results in a phenotype mimicking the human type III osteogenesis imperfecta (small body weight, skeletal deformities and brittle bones) [47].

Starting at 3 weeks of age (just after weaning), 12 mice from each genotype group (vibrated groups: Wild vib and oim vib) were placed into a custom built WBV transparent plastic cage for 15 min per day, 5 days in a week during 5 weeks. The cage was vibrated vertically at a frequency of 45 Hz and a peak acceleration of ± 0.3 g. This vibration regimen was demonstrated to be osteogenic on young growing mice [38] and [39]. The vibration cage had 8 slots (10 ∗ 10 cm each so that 8 mice could vibrate simultaneously) and was mounted on a linear electromagnetic actuator (LAL95-015-70F linear actuator and LAC-1 controller, SMAC Europe Ltd., UK). The linear actuator provided a sinusoidal vertical movement and was force-controlled by a custom made LabVIEW program (NI Corporation Ltd., USA) via a laptop computer and a digital acquisition card (NI USB-6211 multifunction DAQ, NI Corporation Ltd., USA). The actuator was powered by a generator (HY3005D-2, Rapid Electronics Ltd., UK). The acceleration was monitored via an accelerometer (DE-ACCM3D, Dimension Engineering LTD, USA) fixed in the middle of the vibrating cage and the force of the actuator was operator-tuned to obtain a maximum peak acceleration of ± 0.3 g.

Hodgekiss and Ho (1997) found that the growth of most red tide algal blooms is optimized at ratios between 6 and 15. Hence, N:P ratios can act as an early warning signal for algal bloom types and frequencies. Based on the N:P ratio Everolimus trend observed in this study, the N:P ratio should be monitored throughout the BSDB and P input should be

reduced in eastern catchments in order to stop the decreasing trend in the N:P ratio found in this study. From our study we can conclude that the socio-economic changes were most likely responsible for the change in nutrient dynamics in the BSDB. This is because of the steady decrease in TN due to changes in the diffuse sources from agricultural activities mainly in the east (HELCOM, 2011). The transition period brought about improvements in farm management practices, which resulted in reduced

nitrogen loads. In contrast to the changes in diffuse nitrogen Vemurafenib datasheet sources, changes in point sources are likely the main driver for the observed trends in TPC presented in this study (consistent with modelling work from Mörth et al., 2007). Negative trends for TPC in the western catchments can be explained by the increasing percentage of wastewater being treated and by the implementation of advanced treatment techniques in municipal and industrial facilities (HELCOM, 2011). Moreover, lifestyle changes such as closure of heavily polluting factories and an increased use of phosphorus-free detergents also helped in reducing phosphorus concentrations in the catchments. However, a substantial increase in TP was found in the eastern catchments. Reduction of P from point-source discharges started only after

the transition period for the eastern countries. Although P loads to the Baltic Sea reduced from 1989 onwards, the major reductions happened after 2005 when Latvia, Lithuania, Estonia and Poland joined the EU (HELCOM, Montelukast Sodium 2011). The large socio-economic transition in the east was accompanied by a change in land cover that also affected nutrient dynamics. Because no data were available on land cover change, land cover for the year 2000 was used. The first factor shows that cultivated and urban areas both have a positive effect on TNC, TNL and TPC, which is logical as these types of land cover are associated with high input of nitrogen and phosphorus due to anthropogenic activities. Furthermore, wetlands, mixed forest and shrubs and herbs have an adverse effect on TNC, TNL and TPC. This inverse relationship to wetlands confirms that wetlands are important for N-retention (Richardson et al., 1997). It is especially important in the more northern catchments (Fig. 2). Jansson et al. (1998) estimated that wetlands in the BSDB retain approximately 5–13% of the annual total amount of nitrogen entering the BSDB.

On the basis of expression of CXCL12-α and -β in two different breast cancer microarray data sets and immunohistochemistry (IHC) of primary breast tumors, Mirisola and

colleagues reported that higher expression levels of CXCL12-α and -β correlate AZD2281 with better disease-free survival [29]. However, a separate high throughput analysis of CXCL12 expression concluded that higher CXCL12 levels correlate with increased metastasis and local recurrence in breast cancer [17]. Determining effects of high versus low CXCL12 on prognosis and disease progression in breast cancer is essential to direct optimal use of therapeutic antibodies and other agents being developed for CXCL12-targeted cancer therapy [30]. Prior genetic analyses of mRNA for CXCL12 isoforms have used microarrays, which frequently lack probes to detect specific isoforms of these genes. However, next-generation sequencing overcomes this limitation. Using bioinformatics analysis of publicly available data sets from The Cancer Genome Atlas (TCGA), we investigated expression of CXCL12 isoforms, as well as CXCR4 and CXCR7 in breast cancer. We then correlated patterns of expression with important molecular

phenotypes, clinical parameters, and outcomes in these patients. These analyses revealed distinct differences in expression for various isoforms of these genes. We show that low levels of expression of CXCL12 correlate with worse prognosis in breast cancer Temsirolimus mw with isoform-specific differences among α, β, γ, and δ isoforms. These data

demonstrate the impact of CXCL12 isoforms in breast cancer and underscore the need to better understand functional differences among these molecules in disease progression and therapy. Publicly available RNA next-generation sequencing and clinical data (844 breast cancer and 104 benign breast samples) were retrieved from TCGA for breast cancer [31]. Additional clinical data such as PAM50 clustering and clinical follow-up for the TCGA were obtained from the UCSC Cancer Genomics Quinapyramine Browser [32]. RNA sequencing data for seven breast cancer cell lines (two samples each) were obtained from the Illumina iDEA database (www.illumina.com). Three of these cell lines have been shown to have metastatic potential (BT20, MDA-MB-231, and MDA-MB-468), and four cell lines have been shown to have no metastatic potential (BT474, MCF7, T47D, and ZR-75-1) [33], [34] and [35]. RNA sequencing reads were aligned to the genome with Tophat [36] using Genome Reference Consortium Human Build 37 (GRCh37 or hg19) (www.ncbi.nlm.nih.gov) as the reference genome. Seven hundred eighty-five of the cancer samples had clinical data from TCGA, and 832 had data from UCSC Cancer Genome Browser. Her2 status was not included as a column, so we calculated it based on the IHC data column.

Lastly, the cancerous and normal biopsies incubated with either uninhibited or inhibited AF350-WGA resulted in greater fluorescence than the control tumor sample that was not incubated with any AF350-WGA. This demonstrates that the

observed fluorescence from tissue stained with the lectin conjugate is not a result of intrinsic tissue autofluorescence at the excitation wavelength of 365nm. Histological analysis revealed that 4/7 patients PF-01367338 chemical structure had stage I cancer, 1/7 had stage II cancer, and 2/7 had stage IV cancer. Of the seven patients, 6/7 exhibited squamous cell carcinoma while 1/7 exhibited dysplasia. All normal biopsies were confirmed to be free from disease. The histological results are summarized in Table 3. Histology pictures for the tissue in Figure 2 can be seen in Figure 3. Here normal tissue was histologically verified (Figure 3A), whereas cancerous tissue was verified as stage I squamous cell carcinoma ( Figure 3B). It should be noted that the effect of AF350 and AF647 SRT1720 lectin binding on H&E staining was tested by comparing lectin labeled slices with unlabeled control slices from the same biopsy set. Comparison of these slices showed no effect of lectin labeling on H&E staining (data not shown). Furthermore, H&E staining was identical for normal and clinically abnormal tissue independent of the degree of staining with Alexa

Fluor lectin conjugates. The use of molecular and biochemical changes as a basis to develop early detection methods of oral cancer 4-Aminobutyrate aminotransferase were explored in this manuscript. The lectin WGA was primarily chosen for this application as it has high affinity for sialic acid and N-acetyl glucosamine residues which are known to be overexpressed in neoplastic tissue due to aberrant glycosylation [13], [14], [29], [30] and [31]. Furthermore, the relative expression of these sialic acid residues in the

epithelium is suggested to be representative of tumor prognosis [16], [18] and [32]. The data presented here demonstrate that WGA fluorophore probes can agglomerate on cancer cells overexpressing these glycomolecules, successfully yielding statistically higher fluorescence in cancerous tissue than normal tissue. Additionally, the WGA fluorophore probes resulted in a higher SNR than tissue UV autofluorescence at 365nm. Furthermore, through inhibitory binding studies with WGA it was shown that the lectin binding is molecularly specific to these glycans since inhibited WGA resulted in decreased tissue fluorescence, highlighting that the WGA is in fact binding to cellular glycans overexpressed in cancerous tissues. Lastly, this experiment showed that fluorescence intensity differences are not due to tissue diffusion variations between normal and tumor tissues (i.e. leaking vasculature or compromised mucosa). Our data demonstrate that the use of WGA fluorophore probes is a significant improvement over current autofluorescent methods.

7 ng/ml selenium, 0.5 μg/ml hydrocortisone, 20 ng/ml epidermal growth factor, 1 mM sodium pyruvate, 10 mM Hepes, 50 units/ml penicillin, 50 mg/ml streptomycin, 2.5 μg/ml amphotericin B, and 50 μg/ml gentamicin. Cell lines were maintained in Dulbecco’s modified Eagle’s medium and supplemented Hydroxychloroquine price with 10% heat-inactivated FBS, 2 mM glutamine, 1 mM sodium pyruvate, 10 mM Hepes, 50 units/ml penicillin, and 50 mg/ml streptomycin and incubated at 37°C in a humidified 5% CO2/air atmosphere. Cells were seeded in 96-well plates at a density of 1500 to 2500 cells per well and treated with vehicle or different concentrations of drugs for 3 days in sextuplicate.

Then, cells were washed with PBS, fixed with 4% formaldehyde, and stained with 0.05% crystal violet for 30 minutes at room temperature. Cells were then washed three times with deionized water, and the wells were completely dried for at least 30 minutes. Cells were lysed with 0.1 M HCl Y-27632 cost and absorbance was determined at 620 nm in a microplate reader (Infinite M200PRO NanoQuant; Tecan Group, Männedorf, Switzerland). Viability of cells was monitored using the trypan blue dye exclusion

method. Cells were suspended in 0.36% agar with appropriate medium in the presence or absence of 17-AAG or NVP-AUY922 and seeded over a 0.6% agar base layer. After 14 days, cells were stained with iodonitrotetrazolium violet and colonies greater than 100 μm were analyzed with a visible light scanner (Image Scanner III; GE Healthcare, Buckinghamshire, United Kingdom) and software Image Quant TL (GE Healthcare Europe GmbH, Freiburg, Germany). Cells were seeded and treated with Fenbendazole 17-AAG or NVP-AUY922 for 24, 48, and 72 hours. Cells were trypsinized, washed with PBS, fixed with 75% cold ethanol at − 20°C for at least 1 hour, treated with 0.5% Triton X-100 and 0.05% RNase A in PBS for 30 minutes, stained with propidium iodide, and analyzed using a flow cytometer (BD FACSCanto; Becton Dickinson & Co, Franklin Lakes, NJ) to determine

cell cycle distribution of DNA content. Cells were seeded, treated with DMSO, 17-AAG, or NVP-AUY922, and lysed in a buffer containing 50 mM Tris (pH 7.4), 1% NP-40, 150 mM NaCl, 40 mM NaF, 1 mM Na3VO4, 1 mM PMSF, and 10 μg/ml protease inhibitor cocktail (Sigma-Aldrich). Protein determinations were performed by the Bradford method (Bio-Rad, Richmond, CA). Then, 50 to 80 μg of protein from each lysate was separated by sodium dodecyl sulfate–polyacrylamide gel electrophoresis, transferred to polyvinylidene difluoride membranes, blocked and incubated with primary antibodies against EGFR, HER2, HER3, HER4, Akt, Hsp90, Hsp70, Mdr-1, MRP1, BRCP1 and NQO1 from Santa Cruz Biotechnology (Santa Cruz, CA), phospho-ERK1/2, ERK1/2, phospho–ribosomal protein S6 (RPS6), and RPS6 from Cell Signaling Technology (Danvers, MA), or β-actin (Sigma-Aldrich).

The supernatants were collected and used to determine the MCP-1 levels. A subgroup of animals was exposed to inhaled LPS (E. coli 026:B6; 0.1 mg/ml; 10 min) or sterile saline (control) for 1 h following the

last in vivo HQ or vehicle exposure using an ultrasonic nebulizer; 8 h later, blood and BALF were obtained in order to quantify total and differential cell numbers. Leukocytes collected from the abdominal aorta blood of vehicle and HQ, exposed or not to LPS were used to quantify the expression levels of l-selectin, β2-integrin, β3-integrin and PECAM-1. Briefly, erythrocytes were lysed by adding ammonium chloride solution (0.13 M) to the samples and leukocytes were recovered after washing with Hank’s balanced salt solution (HBSS). In order to quantify the expression of adhesion molecules,

this website leukocytes (1 × 105) were incubated for 20 min in the dark at 4 °C with monoclonal antibody (β2 or β3-integrin conjugated with FITC or l-selectin or PECAM-1 conjugated with PE). Following this, the cells were analysed in a FACSCalibur Flow Cytometer (Becton & Dickinson, San Jose, CA, USA). Data from 10,000 events were obtained and only the morphologically viable mononuclear NSC 683864 chemical structure cells were considered for analysis. Flow cytometry standard (FCS) files were analysed using FlowJo software 8.7.1 (Treestar, Ashland, OR, USA). The results were presented as arbitrary units of fluorescence. The concentrations of MCP-1 were measured in the BALF and the supernatant of tracheal tissue or AM cultures using enzyme-linked

immunosorbent assay (ELISA) kits according to the manufacturer’s specifications. The results were expressed as pg/ml. Total RNA was extracted from in vitro Cytidine deaminase LPS-stimulated trachea using Trizol reagent and following the manufacturer’s instructions. The RNA extraction was carried out in an RNAse-free environment and quantified by reading the absorbance at 260 nm. The cDNA was synthesized from total RNA (2 μg) using an oligo(dT)15 primer (20 μg/ml) after incubation (70 °C, 5 min) in the presence of a deoxynucleotide triphosphate mixture (dNTP, 2 mM), a ribonuclease inhibitor (20 U) and Moloney murine leukaemia virus reverse transcriptase (200 U) in reverse transcriptase buffer (25 μl final volume). The reverse transcription occurred during incubation at 42 °C (60 min). For PCR, the cDNA obtained was incubated with Taq DNA polymerase (2.5 U), 3′- and 5′-specific primers (0.4 μM) and dNTP mix (200 μM) in buffer-thermophilic DNA polymerase containing MgCl2 (1.5 mM).

The study was conducted according to the Declaration of Helsinki, with approval of the local ethical committee. All subjects had normal or corrected-to-normal vision. No subject had a history of neurological, major medical, or psychiatric disorder. All participants were right-handed as assessed by the Edinburgh handedness questionnaire (Oldfield, 1971; mean score = 92). The experimental task was similar to the one reported in Engbert et al. (2007). It comprised an active and a passive condition. In the active DNA Synthesis inhibitor condition participants saw a green hash on the screen and pressed a button with their right index finger at

an (unspeeded) time of their own choosing. In the passive condition, a red hash was presented on the screen. The experimenter then pressed the participant’s finger down onto the button, attempting to match the response time of the participants as precisely as possible. Each button press elicited the presentation of a tone after either 200, 300 or 400 msec. Immediately after hearing the tone, participants judged the duration of the interval between the button press and the tone onset using a visual-analogue scale operated with two keys in their left hand (index finger meant that the cursor moved to the left, middle finger

meant that the cursor moved to the right and the middle finger of the right Selleck Duvelisib hand accepted the position of the cursor). Participants were given as much time as they needed for their judgement. The endpoints of the scale were 100 and 500 msec. Prior to scanning participants were trained to discriminate between two tones that were separated by 100 msec and separated by 500 msec for 10 min, with a further 10 min of identical training being given in the scanner prior to the experimental task itself. The trials were presented with a variable inter-trial Morin Hydrate interval ranging from

3000 to 5500 msec. The task consisted of two blocks each containing altogether 30 active and passive trials that were randomly presented. An equal number of trials in all six conditions were presented within each block. Repeated-measures ANOVA with the factors agent (active vs passive) and tone delay (200, 300, 400 msec) was performed on the judgement error, namely the difference between judged time and actual tone delay. Images were collected with a 3 T Magnetom Trio MRI scanner system (Siemens Medical Systems, Erlangen, Germany) using an eight-channel radiofrequency head coil. First, high-resolution anatomical images were acquired using a T1-weighted 3D MPRAGE sequence (TR = 2530 msec, TE = 2.58 msec, TI = 1100 msec, acquisition matrix = 256 × 256 × 176, sagittal FOV = 220 mm, flip angle = 7°, voxel size = .86 × .86 × .9 mm3). Whole brain functional images were collected using a T2*-weighted EPI sequence sensitive to BOLD contrast (TR = 2000 msec, TE = 35 msec, image matrix = 64 × 64, FOV = 224 mm, flip angle = 80°, slice thickness = 3.0 mm, distance factor = 17%, voxel size 3.5 × 3.