Semisolid Enteral Nutrients Alter the Pharmacokinetics of Orally Administered Levetiracetam in Rats.

Enteral nutrients (ENs) affect the plasma drug concentration of orally co-administered drugs, particularly those of antiepileptic drugs, such as phenytoin and carbamazepine. However, few studies have reported the interactions of levetiracetam (LEV), an upcoming antiepileptic drug, with ENs. In this study we aimed to investigate the pharmacokinetics of LEV in 55 rats after oral co-administration of LEV with liquid or semisolid ENs. Compared with the control group, co-administration with Terumeal ® Soft significantly decreased the plasma LEV concentration at 0.5, 1, and 2 h and area under the plasma concentration-time curve from 0 to 3 h (AUC0→3h) (P < 0.01). However, the AUC0→3h of LEV remained unchanged following the administration of Terumeal ® Soft 2 h after the initial LEV administration. Moreover, co-administration with semisolid Racol® NF delayed the absorption of LEV without decreasing the AUC0→3h, whereas liquid Racol ® NF did not alter LEV pharmacokinetics. Thus, co-administration of LEV with Terumeal® Soft reduced the absorption of LEV from the gastrointestinal tract, which was prevented by administering Terumeal ® Soft 2 h after LEV administration. Semisolid Racol ® NF altered LEV pharmacokinetics without decreasing its gastrointestinal absorption. Our findings suggested that careful monitoring of the plasma LEV levels is necessary when co-administering LEV with Terumeal ® Soft, semisolid Racol ® NF, or any other semisolid ENs, to prevent the inadvertent effects of the interaction between LEV and ENs.

Fast electrical control of single electron spins in quantum dots with vanishing influence from nuclear spins.

We demonstrate fast universal electrical spin manipulation with inhomogeneous magnetic fields. With fast Rabi frequency up to 127 MHz, we leave the conventional regime of strong nuclear-spin influence and observe a spin-flip fidelity >96%, a distinct chevron Rabi pattern in the spectral-time domain, and a spin resonance linewidth limited by the Rabi frequency, not by the dephasing rate. In addition, we establish fast z rotations up to 54 MHz by directly controlling the spin phase. Our findings will significantly facilitate tomography and error correction with electron spins in quantum dots.

Two-qubit gate of combined single-spin rotation and interdot spin exchange in a double quantum dot.

A crucial requirement for quantum-information processing is the realization of multiple-qubit quantum gates. Here, we demonstrate an electron spin-based all-electrical two-qubit gate consisting of single-spin rotations and interdot spin exchange in a double quantum dot. A partially entangled output state is obtained by the application of the two-qubit gate to an initial, uncorrelated state. We find that the degree of entanglement is controllable by the exchange operation time. The approach represents a key step towards the realization of universal multiple-qubit gates.

Transcription factor AP-2beta inhibits expression and secretion of leptin, an insulin-sensitizing hormone, in 3T3-L1 adipocytes.

BACKGROUND: We have previously reported an association between the activator protein-2beta (AP-2beta) transcription factor gene and type 2 diabetes. This gene is preferentially expressed in adipose tissue, and subjects with a disease-susceptible allele of AP-2beta showed stronger AP-2beta expression in adipose tissue than those without the susceptible allele. Furthermore, overexpression of AP-2beta led to lipid accumulation and induced insulin resistance in 3T3-L1 adipocytes. RESULT: We found that overexpression of AP-2beta in 3T3-L1 adipocytes decreased the promoter activity of leptin, and subsequently decreased both messenger RNA (mRNA) and protein expression and secretion. Furthermore, knockdown of endogenous AP-2beta by RNA-interference increased mRNA and protein expression of leptin. Electrophoretic mobility shift and chromatin immunoprecipitation assays revealed specific binding of AP-2beta to leptin promoter regions in vitro and in vivo. In addition, site-directed mutagenesis of the AP-2-binding site located between position +34 and +42 relative to the transcription start site abolished the inhibitory effect of AP-2beta. Our results clearly showed that AP-2beta directly inhibited insulin-sensitizing hormone leptin expression by binding to its promoter. CONCLUSION: AP-2beta modulated the expression of leptin through direct interaction with its promoter region.

Visualization of in vivo electroporation-mediated transgene expression in experimental tumors by optical and magnetic resonance imaging.

In vivo electroporation (EP) is an efficient method for effective gene transfer and is highly expected for application in anticancer gene therapy. Non-invasive monitoring of gene transfer/expression is critical for optimal gene therapy. Here we report in vivo optical and high-field magnetic resonance imaging (MRI) of EP-mediated transgene expression in a tumor model. Initially, we observed spatio-temporal change in in vivo EP-mediated transgene expression by optical imaging using red fluorescence protein (RFP) as a reporter gene. Next, we constructed a dual-reporter plasmid carrying a gene-encoding MRI reporter ferritin heavy chain and RFP gene to visualize the intratumoral transgene expression by dual modality. Cells transfected with this plasmid showed lower signal intensity on in vitro T(2)-weighted cellular MRI and quantitatively increased the transverse relaxation rate (1/T(2)) compared with control cells. After conducting in vivo EP in an experimental tumor, the plasmid-injected region showed both fluorescent emissions in optical imaging and detectably lowered signal on T(2)-weighted MRI. The correlative immunohistological findings confirmed that both the reporter transgenes were co-expressed in this region. Thus, our strategy provides a platform for evaluating EP-mediated cancer gene therapy easily and safely without administering contrast agent or substrate.

Antigenic stimulation with cytochrome P450 2J expressed in mouse hepatocellular carcinoma cells regulates host anti-tumour immunity.

Cytochrome P450 2J subfamily (CYP2J) enzymes expressed in mouse hepatocellular carcinoma (HCC) cells were identified as an antigen recognized by specific CD4(+) T cells and the structure of its T cell epitope was determined by proteomics-based exploration. The major histocompatibility complex (MHC) class II binding peptides were isolated from I-A(k)/peptide complex of dendritic cells (DCs) loaded or unloaded with MIH-2 mouse HCC cells. MHC class II-binding peptides found in MIH-2-loaded DCs but not in unloaded DCs were determined by tandem mass spectrometric analysis. The peptide, consisting of amino acid 276-290 (DFIDAFLKEMTKYPE) of mouse CYP2J enzymes, was identified as an antigenic peptide presented in the context of MHC class II. Preventive treatment of mice with CYP2J peptide stimulated interferon (IFN)-gamma production of splenocytes and suppressed the growth of implanted CYP2J-positive MIH-2 cells but not CYP2J-negative murine bladder tumour cells. However, continuous treatment of MIH-2-bearing mice with CYP2J peptide significantly suppressed IFN-gamma production of splenocytes and accelerated the growth of implanted MIH-2 tumours in vivo. Increased frequencies of CD4(+)forkhead box P3 regulatory T cells and CD11b(+)Gr-1(+) myeloid suppressor cells were observed in splenocytes from the continuously immunized mice. These results indicate that antigenecity of CYP2J isoforms expressed in HCC cells activate host anti-tumour immunity at an initial stage of HCC, but suppress host anti-tumour immunity with excessive antigenic stimulation at an advanced stage.

Degeneration of patellar cartilage in patients with recurrent patellar dislocation following conservative treatment: evaluation with delayed gadolinium-enhanced magnetic resonance imaging of cartilage.

OBJECTIVE: To examine the characteristics of cartilage degeneration in patients with recurrent patellar dislocation (RPD) following conservative treatment using delayed gadolinium-enhanced magnetic resonance imaging (MRI) of cartilage (dGEMRIC). DESIGN: This study evaluated three groups of knees: group I, 35 knees from both knees of patients with bilateral RPD and dislocated side knees of patients with unilateral RPD; group II, 15 non-dislocated side knees of patients with unilateral RPD; and group III, 20 knees from both knees of healthy volunteers. Differences in post-contrast T1 [T1(Gd)] of cartilage at both medial and lateral facets between groups I, II and III were analyzed. For group I, possible relationships were evaluated between T1(Gd) of cartilage and patient age, length of time between the initial dislocation and MRI and the total number of dislocations between the initial dislocation and MRI for both medial and lateral facets. RESULTS: The mean T1(Gd) of cartilage at medial facets for groups I, II and III were 411+/-46ms, 465+/-38ms and 490+/-29ms, respectively; there were significant differences between these means (P<0.05). The mean T1(Gd) of cartilage at lateral facets for groups I, II and III were 426+/-53ms, 466+/-45ms and 510+/-36ms, respectively; there were also significant differences between these means (P<0.05). Significant correlations were observed between T1(Gd) of cartilage for both medial and lateral facets and length of time between the initial dislocation and MRI (P<0.05). No other correlations were significant. CONCLUSION: dGEMRIC may be a useful method to monitor glycosaminoglycan concentration in patients with RPD following conservative treatment.

A motif-based profile scanning approach for genome-wide prediction of signaling pathways.

The rapid increase in genomic information requires new techniques to infer protein function and predict protein-protein interactions. Bioinformatics identifies modular signaling domains within protein sequences with a high degree of accuracy. In contrast, little success has been achieved in predicting short linear sequence motifs within proteins targeted by these domains to form complex signaling networks. Here we describe a peptide library-based searching algorithm, accessible over the World Wide Web, that identifies sequence motifs likely to bind to specific protein domains such as 14-3-3, SH2, and SH3 domains, or likely to be phosphorylated by specific protein kinases such as Src and AKT. Predictions from database searches for proteins containing motifs matching two different domains in a common signaling pathway provides a much higher success rate. This technology facilitates prediction of cell signaling networks within proteomes, and could aid in the identification of drug targets for the treatment of human diseases.

Quiet T1-Weighted Pointwise Encoding Time Reduction with Radial Acquisition for Assessing Myelination in the Pediatric Brain.

BACKGROUND AND PURPOSE: T1-weighted pointwise encoding time reduction with radial acquisition (PETRA) sequences require limited gradient activity and allow quiet scanning. We aimed to assess the usefulness of PETRA in pediatric brain imaging. MATERIALS AND METHODS: We included consecutive pediatric patients who underwent both MPRAGE and PETRA. The contrast-to-noise and contrast ratios between WM and GM were compared in the cerebellar WM, internal capsule, and corpus callosum. The degree of myelination was rated by using 4-point scales at each of these locations plus the subcortical WM in the anterior frontal, anterior temporal, and posterior occipital lobes. Two radiologists made all assessments, and the intra- and interrater agreement was calculated by using intraclass correlation coefficients. Acoustic noise on MPRAGE and PETRA was measured. RESULTS: We included 56 patients 5 days to 14 years of age (mean age, 36.6 months) who underwent both MPRAGE and PETRA. The contrast-to-noise and contrast ratios for PETRA were significantly higher than those for MPRAGE (P < .05), excluding the signal ratio for cerebellar WM. Excellent intra- and interrater agreement were obtained for myelination at all locations except the cerebellar WM. The acoustic noise on PETRA (58.2 dB[A]) was much lower than that on MPRAGE (87.4 dB[A]). CONCLUSIONS: PETRA generally showed better objective imaging quality without a difference in subjective image-quality evaluation and produced much less acoustic noise compared with MPRAGE. We conclude that PETRA can substitute for MPRAGE in pediatric brain imaging.

Akt/protein kinase B prevents injury-induced motoneuron death and accelerates axonal regeneration.

Motoneurons require neurotrophic factors for their survival and axonal projection during development, as well as nerve regeneration. By using the axotomy-induced neuronal death paradigm and adenovirus-mediated gene transfer, we attempted to gain insight into the functional significances of major growth factor receptor downstream cascades, Ras-extracellular signal-regulated kinase (Ras-ERK) pathway and phosphatidylinositol-3 kinase-Akt (PI3K-Akt) pathway. After neonatal hypoglossal nerve transection, the constitutively active Akt-overexpressing neurons could survive as well as those overexpressing Bcl-2, whereas the constitutively active ERK kinase (MEK)-overexpressing ones failed to survive. A dominant negative Akt experiment demonstrated that inhibition of Akt pathway hastened axotomy-induced neuronal death in the neonate. In addition, the dominant active Akt-overexpressing adult hypoglossal neurons showed accelerated axonal regeneration after axotomy. These results suggest that Akt plays dual roles in motoneuronal survival and nerve regeneration in vivo and that PI3K-Akt pathway is probably more vital in neuronal survival after injury than Ras-ERK pathway.

Protective effect of imidaprilat, an angiotensin-converting enzyme inhibitor on *OH generation in rat myocardium.

We used a flexibly mounted microdialysis technique to the hearts of rats and examined the protective effect of imidaprilat, an angiotensin-converting enzyme (ACE) inhibitor, on the production of hydroxyl free radical (*OH) generation. A microdialysis probe was implanted into the left ventricular myocardium, and dialysate norepinephrine (NE) concentrations were measured as an index of myocardial interstitial NE levels. Sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was directly infused through a microdialysis probe to detect the generation of *OH reflected by the formation of dihydroxybenzoic acid (DHBA) in rat myocardium. When tyramine (1 mM) was directly infused through the microdialysis probe, the level of NE significantly increased in the dialysate and the level of NE increased by 128 +/- 43%. Imidaprilat (5, 25 and 50 microM) decreased the level of tyramine (1 mM)-induced NE in a concentration-dependent manner. Tyramine clearly produced an increase in *OH formation. In the presence of imidaprilat (50 microM), tyramine failed to increase both 2,3- and 2,5-dihydroxylation. Therefore, the effects of imidaprilat on the *OH generation in the sympathetic nerve blockaded hearts by reserpine treatment were not observed. Moreover, to examine the effect of imidaprilat on *OH formation by ischemia/reperfusion of the myocardium, the heart was subjected to myocardial ischemia for 15 min by occlusion of the left anterior descending coronary artery. When the heart was reperfused, elevation of NE and 2,3- and 2,5-DHBA in imidaprilat (50 microM)-pretreated animals was not observed in the heart dialysate. Imidaprilat 2.5 mg/kg i.p. pretreatment at 5 h before coronary occlusion significantly blunted the rise of serum creatine phosphokinase and improved the electrocardiogram 2 h after coronary occlusion. These results suggest that imidaprilat, an ACE inhibitor, is associated with cardioprotective effect due to the suppression of NE-induced *OH generation.

Protective effect of histidine on para-nonylphenol-enhanced hydroxyl free radical generation induced by 1-methyl-4-phenylpyridinium ion (MPP+) in rat striatum.

The present study examined the antioxidant effect of histidine, a singlet oxygen ((1)O(2)) scavenger, on para-nonylphenol (an environmental estrogen-like chemical)-enhanced hydroxyl radical (.OH) generation induced by 1-methyl-4-phenylpyridinium ion (MPP+) in extracellular fluid of rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was infused through a microdialysis probe to detect the generation of.OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum. Introduction of para-nonylphenol (10 microM) significantly enhanced MPP+ -induced.OH generation. Histidine (25 mM) decreased the para-nonylphenol-enhanced.OH formation. Although the level of MPP+ -induced.OH formation trapped as DHBA after para-nonylphenol treatment increased, para-nonylphenol failed to increase either the level of dopamine and DHBA formation in the reserpinized animals. These results indicate that para-nonylphenol and MPP+ -enhanced.OH generation was based on 1O(2) production, and histidine may have a preventive effect on para-nonylphenol and MPP+ -induced.OH generation in rat striatum.

Effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on nitric oxide-induced hydroxyl radical generation in the rat heart.

We examined the effect of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the production of hydroxyl radical (*OH) generation via nitric oxide synthase (NOS) activation by an in vivo microdialysis technique. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and tissue was perfused with Ringer's solution through the microdialysis probe at a rate of 1 microl/min. Sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was infused directly through a microdialysis probe to detect the generation of *OH. Induction of [K(+)](o) (70 mM) or tyramine (1 mM), significantly increased the formation of *OH trapped as 2,3-dihydroxybenzoic acid (DHBA). The application of N(G)-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, significantly decreased the K(+) depolarization-induced *OH formation, but the effect of tyramine significantly increased the level of 2,3-DHBA. When fluvastatin (100 microM), an inhibitor of low-density lipoprotein (LDL) oxidation, was administered to L-NAME-pretreated animals, both KCl and tyramine failed to increase the level of 2,3-DHBA formation. The effect of fluvastatin may be unrelated to K(+) depolarization-induced *OH generation. To examine the effect of fluvastatin on ischemic/reperfused rat myocardium, the heart was subjected to myocardial ischemia for 15 min by occlusion of the left anterior descending coronary artery (LAD). When the heart was reperfused, a marked elevation of the level of 2,3-DHBA was observed. However, in the presence of fluvastatin (100 microM), the elevation of 2,3-DHBA was not observed in ischemia/reperfused rat heart. Fluvastatin, orally at a dose of 3 mg/kg/day for 4 weeks, significantly blunted the rise of serum creatine phosphokinase and improved the electrocardiogram 2 h after coronary occlusion. These results suggest that fluvastatin is associated with a cardioprotective effect due to the suppression of noradrenaline-induced *OH generation by inhibiting LDL oxidation in the heart.

Pyruvate improves deleterious effects of high glucose on activation of pentose phosphate pathway and glutathione redox cycle in endothelial cells.

In our previous study (Diabetes 44:520-526, 1995), endothelial cells cultured in high glucose condition showed impairment of an oxidant-induced activation of the pentose phosphate pathway (PPP) and a reduced supply of NADPH to the glutathione redox cycle. To gain insight into the mechanisms of this impairment, the protective effect of pyruvate was studied in human umbilical vein endothelial cells cultured in either 5.5 mmol/l glucose (normal glucose [NG] condition) or 33 mmol/l glucose (high glucose [HG] condition). Through pretreatment of cells with 0.2 mmol/l pyruvate for 5-7 days in the HG condition, glucose oxidation through the PPP and total cellular NADPH content in the presence of 0.2 mmol/l H2O2 were increased by 54 (P < 0.05) and 34%, respectively, and glutathione-dependent degradation of H2O2 in HG cells was enhanced by 41% (P < 0.01), when compared with those cells to which pyruvate was not added. The addition of pyruvate significantly reduced the fructose 1,6-bisphosphate (FDP) content and free cytoplasmic NADH/NAD ratio, estimated by increased pyruvate/lactate ratio in NG and HG cells exposed to H2O2. Furthermore, the addition of pyruvate also showed a 46% reduction (P < 0.01) of endothelial cell damage induced by H2O2 in HG cells. These results indicate that abnormalities in PPP activation and glutathione redox cycle activity induced by H2O2 in HG cells are compensated, and that the accentuated reductive stress is improved by an addition of pyruvate. These pyruvate effects are associated with protection against an oxidant-induced endothelial cell injury in the high glucose condition.

Thyroid hormone action: induction of morphological changes and stimulation of cell growth in rat pituitary tumor GH3 cells.

The effects of thyroid hormones on morphology and growth were studied in rat pituitary tumor GH3 cells using medium containing serum depleted of thyroid hormones. T3 and T4 induce the cells to change from a flattened fibroblastic morphology to a rounded or spindle-shaped morphology. The induction in morphological changes is T3 and T4 specific and dose dependent. Thyronine and rT3 are ineffective in inducing morphological changes; the half-maximal effective concentrations for T3 and T4 are 0.3 and 2 nM, respectively. Concomitantly, T3 stimulates cell growth, as indicated by a 2-fold reduction in doubling time and a 2-fold increase in mitotic rate. The growth-stimulating effect has the same analog specificity and dose dependency as the morphological changes. The morphological changes could be potentially useful for evaluating the biological effects of T3 and its analogs and in studying the mechanism of thyroid hormone action.

Antibodies against the human cellular 3,3',5-triiodo-L-thyronine-binding protein (p 58).

High-titer antibodies against a cellular thyroid hormone-binding protein (Mr 58,000, p58) were developed by a special immunization method. To enhance immune responses, this method uses a boosting protocol in which repeated injections of small amounts of antigen are administered at 2-day intervals. Antibodies were detected 1 week after the last injection of antigen by ELISA, Western dot blotting and immunoprecipitation. The anti-p58 antibodies recognized p58 which is bound to the thyroid hormone. With the availability of anti-p58 antibodies, it has become possible to study cellular localization and function.

Intracranial microdialysis of salicylic acid to detect hydroxyl radical generation through dopamine autooxidation in the caudate nucleus: effects of MPP+.

Ringer's solution containing salicylic acid (5 nmol/microliters/min) was infused directly through an intracranial microdialysis probe to detect the generation of hydroxyl radicals (.OH) reflected by the formation of dihydroxybenzoic acids (DHBA) in the caudate nucleus of anesthetized rats. Brain dialysate was assayed for dopamine, 2,3-, and 2,5-DHBA by a high-pressure liquid chromatography-electrochemical (HPLC-EC) procedure. 1-Methyl-4-phenylpyridinium ions (MPP+, 0 to 150 nmol) increased dose-dependently the release of dopamine and the formation of DHBA. A positive linear correlation between the release of dopamine and the formation of 2,3- or 2,5-DHBA was observed (R2 = .98). The present results demonstrate the validity of the use of not only 2,3-DHBA but also 2,5-DHBA as an in vivo index of oxidative damage generated by reactive .OH radicals. In conclusion, the present study demonstrates a novel use of intracranial microdialysis of salicylic acid to assess the oxidative damage elicited by .OH in living brain.

Evaluation of antitumour effects of docetaxel (Taxotere) on human gastric cancers in vitro and in vivo.

In vitro antitumour effects of docetaxel (Taxotere) were examined in nine cultured human gastric cancer cell lines and 18 clinical gastric cancer specimens. In vivo antitumour effects were examined in human gastric cancer xenografts in nude mice. The activity was compared with paclitaxel (Taxol). Docetaxel was more effective than paclitaxel in six of the nine cell lines and the effectiveness rates of docetaxel and paclitaxel were 56% (10/18) and 6% (1/17), respectively, in the clinical gastric cancer specimens. In vivo docetaxel showed superior antitumour effect on well differentiated (MKN-28), poorly differentiated (MKN-45) and undifferentiated (KKLS) gastric cancer xenografts. We conclude that docetaxel promises to be clinically active against gastric carcinomas.

New potent antagonists of leukotrienes C4 and D4. 1. Synthesis and structure-activity relationships.

(p-Amylcinnamoyl)anthranilic acid (3a) had moderate antagonist activities against LTD4-induced smooth muscle contraction on guinea pig ileum and LTC4-induced bronchoconstriction in anesthetized guinea pigs. Modifications were made in the hydrophobic part (cinnamoyl moiety) and the hydrophilic part (anthranilate moiety) of 3a. A series of 8-(benzoylamino)-2-tetrazol-5-yl-1,4-benzodioxans and 8-(benzoylamino)-2-tetrazol-5-yl-4-oxo-4H-1-benzopyrans were revealed to be potent antagonists of leukotrienes C4 and D4. Among both series, ONO-RS-347 (18k) and ONO-RS-411 (19h) were the most potent and orally active antagonists, respectively. Structure-activity relationships are discussed.

Long-term assessment of posttransplant renal prognosis with 31 P magnetic resonance spectroscopy.

BACKGROUND: 31P-magnetic resonance spectroscopy (MRS) has been widely used to study pretransplantation renal viability, and although some had discussed posttransplant renal viability, no one has examined long-term posttransplant renal prognosis. We discuss the use of 31P-MRS to assess the long-term prognosis from the time when MRS was performed. METHODS: We studied 20 patients with renal allografts. 1.5 Tesla clinical magnetic resonance imaging (MRI) and 15 cm surface coil was used for 31P-MRS. Localized 31P-MRS was done using image selected in vivo spectroscopy (ISIS) method. Individual peaks were fitted by Lorenzian line-shapes with a least square method and peak area ratios were calculated. RESULTS: A beta-adenosine triphosphate/inorganic phosphate (beta-ATP/Pi) ratio >1.2 had sensitivity of 92.8%, specificity of 100%, and accuracy of 95% for predicting 3-year renal survival; a beta-ATP/Pi ratio >1.2 had sensitivity of 90.9%, specificity of 66.7%, and accuracy of 76.9% for predicting 5-year renal survival. We compared 31P-MRS spectra data between the survived group and failed group. The survived group had significantly higher beta-ATP/Pi, alpha-ATP/Pi, and phosphodiester (PDE)/Pi ratios than the failed group. CONCLUSIONS: We discussed the beta-ATP/Pi value as a parameter for predicting long-term survival of a transplanted kidney from the time when MRS was performed. A value above 1.2 suggests a high probability of 3-year renal survival, whereas a value over 2.5 indicates that the transplanted kidney could survive over 5 years. 31P-MRS may be useful for predicting long-term survival of transplanted kidneys, but additional studies are needed.