Biomedical subjects

Y Yu

Publications and source records attributed to Y Yu.

At least 307 records · Page 17Linked to original sources

PubMed1998

Modulation of endoplasmic reticulum calcium pump by Bcl-2.

Members of the bcl-2 gene family encode proteins that function either to promote or to inhibit apoptosis. Despite numerous efforts, the mechanism of action of Bcl-2, an anti-apoptotic protein, is still not clear. In particular, the relation between Bcl-2 and the endoplasmic reticulum (ER) calcium store is not well-understood. In the present work, we examined the effect of Bcl-2 on the ER store. We demonstrate that overexpression of Bcl-2 in breast epithelial cells modulates ER store by upregulating calcium pump (SERCA) expression without affecting the release channel (IP3R). The steady state levels of SERCA2 mRNA and protein were both increased in Bcl-2 expression clones. The increase in SERCA2 protein leads to accelerated calcium uptake and enhanced Ca2+ loading. In addition, we also show the detection of intracellular interaction between Bcl-2 and SERCA molecules by co-immunoprecipitation. Since high lumenal Ca2+ concentration of ER is essential for normal cell functions, the results suggest that Bcl-2 preserves the ER Ca2+ store by upregulating SERCA gene expression as well as by a possible interaction with the pump.

Calcium↗

PubMed1998

Molecular events after antisense inhibition of hMSH2 in a HeLa cell line.

To establish a cause-effect relationship between the human mismatch repair pathway deficiency and the observed phenotypes, a hMSH2 deficient HeLa cell line (HeLa-MSH2-) was established by transfecting the HeLa cells with an antisense RNA expression plasmid. The expression plasmid was constructed by inserting an 851 bp fragment of hMSH2 cDNA into the polyclonal site of the vector pREP9 in a reversed orientation. The production of the mismatch binding protein, hMSH2, was inhibited in HeLa-MSH2- cells, as demonstrated by Western blotting and band shift assay of its whole cell extract. The growth rate of this cell line was not different from the parental HeLa cells soon after transfection. However, the rate was faster after 10 subcultures. The spontaneous mutation frequency at the hypoxanthine phosphoribosyltransferase (HPRT) locus increased markedly, but no N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) tolerance appeared in this cell line. Our results clearly demonstrated several molecular events happened after the inhibition of a major mismatch recognition protein, hMSH2, in the mismatch repair pathway, mimicking carcinogenesis processes.

Base Pair Mismatch↗

PubMed1998

Effects of ZD6169, a KATP channel opener, on bladder hyperactivity and spinal c-fos expression evoked by bladder irritation in rats.

Cystometrographic recording and immunocytochemical techniques were used to examine the effects of ZD6169, an ATP-sensitive K+-channel opener, and capsaicin, an afferent neurotoxin, on urinary bladder hyperactivity and immediate early gene expression in the spinal cord induced by acetic acid (0.25%) irritation of the bladder. Chemical irritation of the bladder of the rat increased the frequency of voiding reflexes by 8 fold and increased c-fos expression in neurons in the dorsal commissure (DCM), sacral parasympathetic nucleus (SPN) as well as the medial and lateral dorsal horn (MDH, LDH) of L6 and S1 segments of the spinal cord. Pretreatment with ZD6169 (30 nM) for 1 h reduced the effect of acetic acid on voiding frequency as reflected by an increase in the intercontraction interval (ICI, 137+/-48% increase, P<0.05). ZD6169 also decreased the number of Fos positive neurons in the L6 spinal cord, in the DCM (62.1+/-7.1% decrease), SPN (48.8+/-7%), MDH (50+/-7.3%) and LDH regions (38. 8+/-10.5%). Similar reductions were noted in the S1 spinal cord: 65. 1+/-10.8% in DCM, 53.8+/-11% in SPN, 56+/-10.4% in MDH and 25.3+/-18. 1% in LDH. Capsaicin pretreatment (125 mg/kg, s.c., 4 days prior to the experiments) also reduced bladder hyperactivity (550% increase in ICI) and decreased the numbers of acetic acid-induced Fos positive neurons 78.8+/-6.3% in DCM, 73+/-7.8% in MDH, 59.2+/-16% in LDH and 45.2+/-17% in SPN of L6 segment of the spinal cord. These results suggest that ZD6169 can influence bladder hyperactivity by suppressing the firing of capsaicin-sensitive C-fiber bladder afferents which are known to modulate the micturition reflex.

Adenosine Triphosphate↗

PubMed1998

Role of endogenous interferon-gamma on the enhancement of splenic NK cell activity by electroacupuncture stimulation in mice.

Successive electro-acupuncture (EA) stimulation applied to bilateral anterior tibial muscles, where Zusanli (ST36) acupoints are located, once a day (30 min) for 3 successive days significantly enhanced splenic natural killer (NK) cell activity in BALB/c mice. The percentage of splenic NK cells, as measured by flow cytometry, was not affected in these mice. Interferon (IFN)-gamma level in splenic aqueous extract, prepared from the ST36 acupoint-stimulated mice, was significantly higher than that of the controls. In vivo treatment with neutralizing monoclonal antibody against mouse IFN-gamma completely abrogated the increase in splenic NK cell activity induced by ST36 acupoint stimulation. The same stimulation also significantly increased the concentration of splenic beta-endorphin, which coincided with the significant increase in splenic IFN-gamma production. Pre-administration of 10 mg/kg naloxone before initiation of EA stimulation every day reduced the enhancements of NK cell activity and IFN-gamma level. These observations strongly suggest that endogenous IFN-gamma mediates the up-regulation of NK cell activity by EA stimulation at the ST36 acupoints. Furthermore, endogenous beta-endorphin secreted by EA stimulation also plays an important role in the up-regulation of NK cell function, which may be realized through regulating IFN-gamma production.

Animals↗

PubMed1998

Prostaglandin E2 stimulates IL-8 gene expression in human colonic epithelial cells by a posttranscriptional mechanism.

Intestinal mucosal epithelial cells produce IL-8, a neutrophil chemoattractant that contributes to mucosal inflammation in various infectious and inflammatory diseases. However, the mediators involved and the molecular regulation of IL-8 production are poorly understood. As PGE2 is central in gut inflammation and modulates a variety of mucosal epithelial cell functions, we determined whether PGE2 can affect the expression of IL-8. Exogenous PGE2 induced the accumulation of IL-8 mRNA and protein production in a dose- and time-dependent manner in T84 human colonic epithelial cells. Forskolin and dibutyryl cAMP, which increase intracellular cAMP, stimulated IL-8 in a fashion similar to that of PGE2. PGE2 and PGE2 receptor agonists coupling through EP4 receptors elevated intracellular cAMP and up-regulated IL-8 mRNA expression by activating protein kinase A. Unlike PMA, PGE2 and forskolin did not increase IL-8 gene transcription. However, PGE2, forskolin, and PMA enhanced the stability of IL-8 mRNA transcripts, suggesting the involvement of posttranscriptional regulation. Chloramphenicol acetyltransferase reporter gene transfection studies confirmed the presence of a PGE2 responsive cis-element(s) in the IL-8 3' untranslated region. Furthermore, dexamethasone inhibited PGE2-, forskolin-, and dibutyryl cAMP-induced, but not PMA-induced, IL-8 protein production. These results highlight a novel role for PGE2 in up-regulating IL-8 gene expression by colonic epithelial cells, which may contribute to exacerbation of inflammation in the gastrointestinal tract.

Adenocarcinoma↗

PubMed1998

p53 is involved in but not required for ionizing radiation-induced caspase-3 activation and apoptosis in human lymphoblast cell lines.

The caspase-3 has been shown to be involved in mediating apoptosis induced by different stimuli. However, it is still unclear whether p53 is required for the ionizing radiation (IR)-induced caspase-3 activation. In the present study, we examined IR-induced apoptosis in three closely related human lymphoblast cell lines that differ in p53 status. Irradiation of TK6 cells (wild-type p53) with 4 Gy gamma-rays resulted in rapid apoptosis, whereas the apoptotic response was delayed and reduced in WTK1 cells (mutant p53) and the TK6 derivative line expressing HPV16 E6 (abrogated p53). The differential apoptotic responses in these cell lines correlated with caspase-3 activation. IR induced an early as well as a late phase of caspase-3 activation in TK6 but only a delayed onset in WTK1 and TK6-E6-5E cells. The early phase of caspase-3 activation coincided with an elevation of p53 and bax protein levels. Pretreatment of all three cell lines with a caspases inhibitor z-VAD-FMK inhibited apoptosis. These results suggest that IR-induced apoptosis is mediated by a mechanism involving the caspase-3 cascade, which is shared by both p53-dependent and -independent pathways. The activation of caspase-3 by IR may thus engage at least two separate mechanisms, one through the regulation of the bcl-2 family members by p53, whereas the other yet-to-be-identified one involves neither p53 nor bax.

Amino Acid Chloromethyl Ketones↗

PubMed1998

Functional expression of a Ca2+-activated K+ channel in Xenopus oocytes injected with RNAs from the rat testis.

The present study investigated the feasibility of using Xenopus oocytes to express sperm ion channel by injection of RNAs extracted from the rat testis. The RNA-injected oocytes expressed an outwardly rectifying current which was dependent on K+ concentration and inhibitable by K+ channel blockers, charybdotoxin (CTX) and tetraethylammonium (TEA). The Ca2+ ionophore, ionomycin, could also stimulate current activation with similar current characteristics in the RNA-injected oocytes, suggesting the expression of a Ca2+-activated K+ channel. Immunolocalization indicated predominant Ca2+-activated K+ channel immunoreactivity associated with spermatogenic cells. Reverse transcriptase-polymerase chain reaction studies confirmed the expression of the Ca2+-activated K+ channel mRNA in isolated spermatogenic cells. Our results suggest that ion channels and/or receptors of spermatogenic cells could be investigated using the Xenopus oocyte as an expression system. The present study also suggests that sperm may possess a Ca2+-activated K+ channel which has been implicated in the process of sperm activation and gamete interaction.

Animals↗

PubMed1998

Solution structure of thermostable cytochrome c-552 from Hydrogenobacter thermophilus determined by 1H-NMR spectroscopy.

The solution structure of a thermostable cytochrome c-552 from a thermophilic hydrogen oxidizing bacterium Hydrogenobacter thermophilus was determined by proton nuclear magnetic resonance spectroscopy. Twenty structures were calculated by the X-PLOR program on the basis of 902 interproton distances, 21 hydrogen bonds, and 13 torsion angle constraints. The pairwise average root-mean-square deviation for the main chain heavy atoms was 0.91 +/- 0.11 A. The main chain folding of the cytochrome c-552 was almost the same as that of Pseudomonas aeruginosa cytochrome c-551 that has 59% sequence identity to the cytochrome c-552 but is less thermostable. We found several differences in local structures between the cytochromes c-552 and c-551. In the cytochrome c-552, aromatic-amino interactions were uniquely formed between Arg 35 and Tyr 32 and/or Tyr 41, the latter also having hydrophobic contacts with the side chains of Tyr 32, Ala 38, and Leu 42. Small hydrophobic cores were more tightly packed in the cytochrome c-552 because of the occupancies of Ala 5, Met 11, and Ile 76, each substituted by Phe 7, Val 13, and Val 78, respectively, in the cytochrome c-551. Some of these structural differences may contribute to the higher thermostability of the cytochrome c-552.

Amino Acid Sequence↗

PubMed1998

Expression of GDNF family receptor components during development: implications in the mechanisms of interaction.

Glial cell line-derived neurotrophic factor (GDNF) and a related factor, neurturin, promote survival of diverse groups of neurons. Both GDNF and neurturin signal via a two-component receptor complex that consists of a ligand-binding GDNF family receptor (GFRalpha-1 or GFRalpha-2) and the receptor protein tyrosine kinase Ret. Recently, a third receptor related to GFRalpha-1 and GFRalpha-2 has also been isolated and designated GFRalpha-3. Although much is known about the interaction among GDNF family factors, Ret, and the alpha-receptors in vitro, it remains unclear about their interactions in vivo. We show here by in situ hybridization that Ret and the alpha-receptors may be colocalized in the same tissues or expressed separately in projecting and target tissues, respectively, indicating that two distinct modes of interaction between Ret and the alpha-receptors exist in vivo. First, Ret may interact with the alpha-receptors expressed in the same cells (termed interaction "in cis") in many tissues and cell populations that respond to GDNF and/or neurturin, such as the substantia nigra, dorsal root ganglia, spinal cord motoneurons, kidney, and intestine. Second, Ret may interact with the alpha-receptors localized in the target neurons (termed interaction "in trans"). In addition, we present evidence in vitro that GFRalpha-1 mediates Ret activation by GDNF in trans. These observations suggest that there are multiple mechanisms regulating the interaction between Ret and the alpha-receptors that mediates the effects of GDNF family trophic factors on the survival and differentiation of cells and on neuron-target interactions in the nervous system.

Aging↗

PubMed1998

An NMR-based identification of peptide fragments mimicking the interactions of the cathepsin B propeptide.

Selected fragments of the 62-residue proregion (or residues 1p-62p) of the cysteine protease cathepsin B were synthesized and their interactions with cathepsin B studied by use of proton NMR spectroscopy. Peptide fragments 16p-51p and 26p-51p exhibited differential perturbations of their proton resonances in the presence of cathepsin B. These resonance perturbations were lost for the further truncated 36p-51p fragment, but remained in the 26p-43p and 28p-43p peptide fragments. Residues 23p-26p or TWQ25A in the N-terminal 1p-29p fragment did not show cathepsin B-induced resonance perturbations although the same residues had strongly perturbed proton resonances within the 16p-51p peptide. Both the 1p-29p and 36p-51p fragments lack a common set of hydrophobic residues 30p-35p or F30YNVDI35 from the proregion. The presence of residues F30YNVDI35 appears to confer a conformational preference in peptide fragments 16p-51p, 26p-51p, 28p-43p and 26p-43p, but the same residues induce the aggregation of peptides 16p-36p and 1p-36p. The peptide fragment 26p-43p binds to the active site, as indicated by its inhibition of the catalytic activity of cathepsin B. The cathepsin B prosegment can therefore be reduced into smaller, but functional subunits 28p-43p or 26p-43p that retain specific binding interactions with cathepsin B. These results also suggest that residues F30YNVDI35 may constitute an essential element for the selective inhibition of cathepsin B by the full-length cathepsin B proregion.

Cathepsin B↗

PubMed1998

Sp1, but not Sp3, functions to mediate promoter activation by TGF-beta through canonical Sp1 binding sites.

Transforming growth factor beta (TGF-beta) causes growth arrest at the G1 phase of the cell cycle in most cell types. Both the cyclin dependent kinase inhibitor p15(INK4B) and p21(Cip1/WAF1) genes have been found to be induced by TGF-beta in human keratinocyte HaCaT cells. Analyses of the human p15 and p21 promoters have led to the identification of GC-rich sequences capable of binding to Sp1 transcription factors as necessary elements for the TGF-beta induction of both promoters. We report here that canonical Sp1 binding sites derived from the SV40 21 bp repeat could also support promoter induction by TGF-beta when placed upstream of a minimal luciferase reporter construct containing only the TATA and Inr elements. Gel retardation assays identified Sp1, Sp3 and DeltaSp3 as major factors binding to the canonical Sp1 sites in HaCaT cells and that TGF-beta treatment did not change their binding activities over a 24 h period. More importantly, GAL4-Sp1, but not GAL4-Sp3, chimeric protein supported TGF-beta mediated gene induction from a luciferase reporter construct driven by five GAL4 DNA binding sites. Our results suggest that Sp1 binding site can function as a distinct TGF-beta responsive element for TGF-beta mediated promoter expression and Sp1 per se can mediate this response.

Adenovirus E1A Proteins↗

PubMed1998

Expression of ADP-ribosyltransferase on normal T lymphocytes and effects of nicotinamide adenine dinucleotide on their function.

ADP-ribosyltransferase (ADPRT) is a glycosylphosphatidylinositol-anchored cell surface enzyme on CTL. Expression of this enzyme correlates with suppression of CTL functions in the presence of its substrate beta-nicotinamide adenine dinucleotide (NAD). To investigate the immunoregulatory importance of ADPRT on normal lymphocytes in vivo, NAD was injected into mice and the effects on cell-mediated and humoral immunity were assessed. Induction of both delayed-type hypersensitivity and CTL, but not Ab responses, are shown to be suppressed by NAD. Consistent with this, mature T cells, but not B cells or macrophages, express ADPRT and are able to ADP-ribosylate cell surface proteins. ADP-ribosylated molecules were identified as LFA-1, CD8, CD27, CD43, CD44, and CD45. Concomitant to ADP-ribosylation of these molecules, T cell trafficking to secondary lymphoid organs is suppressed by NAD. To examine whether this is due to effects of NAD on cell activation, Ag-stimulated responses were assayed in vitro. NAD is shown to inhibit induction of cell proliferation, cytotoxicity, and cytokine secretion. It is suggested that ADPRT regulates T cells on the level of transmembrane signaling via ADP-ribosylation of cell surface molecules. This effect is reported to be indirect, as it involves transmission of signals through TCRs, which are not ADP-ribosylated.

Animals↗

PubMed1998

Absence of a radiation-induced first-cycle G1-S arrest in p53+ human tumor cells synchronized by mitotic selection.

It is well known that normal human diploid fibroblasts undergo a significant, p53-dependent arrest in the G1 phase of the cell cycle after exposure to ionizing radiation. The presence and magnitude of a G1 arrest in human tumor cell lines, however, has been controversial, particularly in cells derived from solid tumors and irradiated during exponential growth. To examine this question more precisely, we synchronized cells by mitotic selection and irradiated them in very early G1 prior to any of the described G1 checkpoints. Progression of cells from G1 into the S phase was monitored by autoradiographic measurement of cumulative labeling indices and by flow cytometric analysis. Three different human tumor cell lines confirmed as expressing normal p53 function were examined, i.e., lines derived from an adenocarcinoma of the colon (RKO), a breast cancer (MCF-7), and a squamous cell carcinoma (SCC61). Following irradiation with 4-8 Gy, there was a transient delay in progression from G1 into S phase, lasting approximately 2 h, and in two of the three cell lines (RKO and MCF-7), a small fraction of cells (5-8%) never entered the first S phase. Although there was no evidence for a prolonged G1 arrest, the expected G2 delay was observed in all three cell lines. When irradiated RKO cells were resynchronized at the next mitosis, approximately 30% of the cells did not enter the second S phase. This latter finding is consistent with earlier reports on the kinetics of radiation-induced reproductive failure in mammalian cells. These results indicate that cells derived from human solid tumors that express normal p53 may respond to irradiation quite differently than do normal cells in terms of G1 checkpoint control.

Adenocarcinoma↗

PubMed1998

Accelerated recovery of irradiation-induced bone marrow depression by fibroblast-mediated interleukin 6 gene therapy in combination with bone marrow transplantation in mice.

BACKGROUND: Both fibroblast-mediated cytokine gene therapy and bone marrow transplantation (BMT) have proven to be efficient protocols for the recovery of bone marrow depression. In this report, the effects of fibroblast-mediated interleukin (IL)-6 gene therapy, in combination with BMT, on the recovery of irradiation-induced bone marrow depression were investigated. METHODS: NIH3T3 fibroblast cells engineered to secrete IL-6 (NIH3T3-IL-6) or NIH3T3 cells transduced with the neomycin gene (NIH3T3-Neo), in combination with 10(7), 10(6), or 10(5) syngeneic bone marrow cells, were implanted into irradiated mice. RESULTS: The platelets and white blood cells in the peripheral blood of the irradiated mice increased greatly 12 days after implantation of NIH3T3-IL-6 cells and BMT, the white blood cell counts were restored to a normal level 32 days after the combined therapy, and the platelet number was obviously higher than that in mice implanted with NIH3T3-Neo and BMT. Twenty and 25 days after the combined therapy, the mice showed accelerated recovery of colony-forming unit (CFU)-granulocyte/macrophages and CFU-megakaryocytes when compared with the mice implanted with NIH3T3-Neo cells and BMT. Ten days after lethal irradiation with gamma rays, the spleens formed more CFU-spleen in mice implanted with NIH3T3-IL-6 cells and BMT than in mice injected with phosphate-buffered saline or NIH3T3-Neo cells. Combined therapy with NIH3T3-IL-6 cell implantation and BMT delayed the survival period of the hematopoietic-depressed mice significantly when compared with therapy with NIH3T3-Neo cell implantation and BMT. CONCLUSIONS: These data demonstrated that the combined therapy of fibroblast-mediated IL-6 gene therapy and BMT could significantly promote the recovery of irradiation-induced hematopoietic depression.

3T3 Cells↗

PubMed1998

MR image-guided portal verification for brain treatment field.

PURPOSE: To investigate a method for the generation of digitally reconstructed radiographs directly from MR images (DRR-MRI) to guide a computerized portal verification procedure. METHODS AND MATERIALS: Several major steps were developed to perform an MR image-guided portal verification procedure. Initially, a wavelet-based multiresolution adaptive thresholding method was used to segment the skin slice-by-slice in MR brain axial images. Some selected anatomical structures, such as target volume and critical organs, were then manually identified and were reassigned to relatively higher intensities. Interslice information was interpolated with a directional method to achieve comparable display resolution in three dimensions. Next, a ray-tracing method was used to generate a DRR-MRI image at the planned treatment position, and the ray tracing was simply performed on summation of voxels along the ray. The skin and its relative positions were also projected to the DRR-MRI and were used to guide the search of similar features in the portal image. A Canny edge detector was used to enhance the brain contour in both portal and simulation images. The skin in the brain portal image was then extracted using a knowledge-based searching technique. Finally, a Chamfer matching technique was used to correlate features between DRR-MRI and portal image. RESULTS: The MR image-guided portal verification method was evaluated using a brain phantom case and a clinical patient case. Both DRR-CT and DRR-MRI were generated using CT and MR phantom images with the same beam orientation and then compared. The matching result indicated that the maximum deviation of internal structures was less than 1 mm. The segmented results for brain MR slice images indicated that a wavelet-based image segmentation technique provided a reasonable estimation for the brain skin. For the clinical patient case with a given portal field, the MR image-guided verification method provided an excellent match between features in both DRR-MRI and portal image. Moreover, target volume could be accurately visualized in the DRR-MRI and mapped over to the corresponding portal image for treatment verification. The accuracy of DRR-MRI was also examined by comparing it to the corresponding simulation image. The matching results indicated that the maximum deviation of anatomical features was less than 2.5 mm. CONCLUSION: A method for MR image-guided portal verification of brain treatment field was developed. Although the radiographic appearance in the DRR-MRI is different from that in the portal image, DRR-MRI provides essential anatomical features (landmarks and target volume) as well as their relative locations to be used as references for computerized portal verification.

Brain Neoplasms↗

PubMed1998

Overproduction of beta-glucosidase in active form by an Escherichia coli system coexpressing the chaperonin GroEL/ES.

beta-Glucosidase from Cellvibrio gilvus was successfully overproduced in soluble form in Escherichia coli, with the coexpression of GroEL/ES. Without the GroEL/ES protein, the beta-glucosidase overexpressed in E. coli constituted a huge amount (80%) of the total cellular protein, but was localized in the insoluble fraction, and little activity was detected in the soluble fraction. Coexpression of the E. coli GroEL/ES had a drastic impact on the proper folding of the beta-glucosidase; 20% of the overexpressed enzyme was recovered in the soluble fraction in active form. In addition, the synergistic effect of GroEL/ES and the low induction temperature led to 70% solubilization of the total expressed target protein and more than a 20-fold increase in activity. Similar effects of GroEL/ES were also observed on the overexpressed beta-glucosidase from Agrobacterium tumefaciens.

Chaperonin 60↗

PubMed1998

Expression of p16 induces transcriptional downregulation of the RB gene.

The RB and p16(INK4A) tumor suppressor genes function in the same pathway of cell cycle control. Previous evidence indicates that the p16(INK4A) gene is transcriptionally repressed by the RB gene product, pRB. In this study using human ovarian cancer cell lines, we found that RB protein and mRNA were expressed at higher levels in cell lines lacking p16 than in those with normal p16. Since this suggests a potential role of p16 in regulating the cellular level of pRB, we studied the effect of wild-type p16(INK4A) on expression of the RB gene. Introduction of p16(INK4A), carried by an adenovirus vector, into p16-negative cell lines dramatically decreased expression of RB protein and mRNA. Nuclei run-off assays demonstrated that p16 expression induced transcriptional downregulation of the RB gene. These results indicate that expression of RB is inversely regulated by p16. The findings reveal a new dimension of pRB-p16 interaction and should have implications for p16(INK4A)-mediated gene therapy.

Adenoviridae↗

PubMed1998

Human magnetic resonance imaging at 8 T.

In this work, we present the first human magnetic resonance image (MRI) obtained at ultrahigh field strengths (8 T). We demonstrate that clinical imaging will be possible at 8 T and that reasonable quality head images can be obtained at this field strength. Most importantly, we emphasize that the power required to excite the spins at 8 T is much lower than had previously been predicted by the nuclear magnetic resonance theory. A 90 degree pulse in the head at 8 T requires only approximately 0.085 J of energy (90 W for a 2-lobe 4 ms sinc pulse). Based on measurements at 4 T, 1-2 J of energy should have been utilized to achieve a 90 degree excitation at 8 T. The fact that the energy required for spin excitation at 8 T is much lower than predicted by the NMR theory, will be extremely important to the viability of ultrahigh field imaging, since concerns related to power absorption and specific absorption rate (SAR) violations at ultrahigh field are alleviated. As such, it will be possible to utilize RF intensive pulse sequences and adiabatic spin excitation at 8 T without significant risk to the subject.

Brain↗