Impaired cardiac response to exercise in post-menopausal women: relationship with peripheral vascular function.

Endothelial dysfunction has been demonstrated in post-menopausal women. To assess the relationship between peripheral vascular reserve and cardiac function during exercise in post-menopausal women, 91 subjects, who had no ischaemic findings on myocardial SPECT, were assigned to four groups: pre-menopausal women (n=13), post-menopausal women (n=33), younger men aged < or =50 years (n=10), and older men aged >50 years (n=35). First-pass radionuclide angiography was performed before and during bicycle exercise to calculate ejection fraction (EF) and peripheral vascular resistance (VR). There were no differences in haemodynamic variables among the groups at baseline. The per cent increase in EF=(exercise EF - resting EF)x100/resting EF, and the per cent decrease in VR=(resting VR - exercise VR)x100/resting VR were depressed in the post-menopausal women (0.4+/-2% and 35+/-3%, respectively) compared to the pre-menopausal women (10+/-3% and 47+/-3%, respectively; P<0.05 each). Although the age dependent impairment is thought to cause this depression, neither the per cent increase in EF nor the per cent decrease in VR in the older men was significantly different from that in the younger men. Post-menopausal women exhibited depressed cardiac function during exercise, which may be related to the impairment of peripheral vascular function after menopause.

Echocardiographic features in a patient with primary oxalosis.

Primary oxalosis is a rare congenital disorder of oxalate metabolism characterized by deposits of calcium oxalate in several organs, including the heart. We present the case of a 38-year-old man with primary oxalosis who had unique echocardiographic findings. Two-dimensional echocardiography revealed the sparkling high intensity echocardiographic pattern and concentric thickening of myocardial walls. Microscopic examinations showed the extensive deposits of calcium oxalate crystals in the myocardium. Therefore, we suggest that primary oxalosis should be given important consideration in the differential diagnosis of a hypertrophied myocardium with high intensity echocardiograms.

Troglitazone enhances glucose uptake induced by alpha-adrenoceptor stimulation via phosphatidylinositol 3-kinase in rat heart.

1. Thiazolidinedione-derived agents have been reported to act as insulin sensitizers by augmenting insulin-dependent stimulation of phosphatidylinositol 3-kinase (PI3K) activity in a specific manner. It has been suggested that alpha-adrenoceptor stimulation mediates glucose uptake through PI3K in the heart. 2. To elucidate whether the thiazolidinedione-derived agent troglitazone (TRO) affects glucose uptake induced by alpha-adrenoceptor stimulation through PI3K, the rate of glucose uptake was quantified from the rate of accumulation of sugar phosphate (d[SP]/dt) using [(31)P] nuclear magnetic resonance spectroscopy after substitution of glucose with 2-deoxyglucose in rat perfused heart. Hearts were stimulated with 100 micromol/L phenylephrine plus 10 micromol/L propranolol (alpha-adrenoceptor stimulation), or 1 micromol/L isoproterenol plus 10 micromol/L phentolamine (beta-adrenoceptor stimulation). 3. The d[SP]/dt in the alpha- and beta-adrenoceptor-stimulated groups (0.45 +/- 0.06 and 0.42 +/- 0.04 micromol/min per g, respectively) was higher than that of the control group (0.27 +/- 0.02 micromol/min per g; P < 0.01). The addition of 2 microg/mL troglitazone to alpha-adrenoceptor stimulation augmented d[SP]/dt (0.72 +/- 0.08 micromol/min per g; P < 0.05 vs the alpha-adrenoceptor-stimulated group), which was effectively blocked by 3 micromol/L wortmannin (0.35 +/- 0.06 micromol/min per g; P < 0.01 vs troglitazone + alpha-adrenoceptor stimulation group). However, addition of troglitazone to beta-adrenoceptor stimulation did not alter d[SP]/dt (0.33 +/- 0.02 micromol/min per g; P = NS vs the beta-adrenoceptor-stimulated group). 4. These results indicate that troglitazone acutely enhances alpha-adrenoceptor stimulation on glucose uptake through a PI3K-dependent pathway, thus possibly improving glucose utilization in a catecholamine-released state.

Role of intracellular Na(+) kinetics in preconditioned rat heart.

To elucidate the role of intracellular Na(+) kinetics in the mechanism for ischemic preconditioning (IPC), we measured intracellular Na(+) concentration ([Na(+)](i)) using (23)Na-magnetic resonance spectroscopy in isolated rat hearts. IPC significantly delayed the initial [Na(+)](i) increase (d[Na(+)](i)/dt) compared with non-IPC control, resulting in attenuation of Na(+) accumulation (Delta[Na(+)](i)) during 27 minutes of ischemia with better functional recovery. [Na(+)](i) in IPC, but not in control, recovered to preischemic level during a 6-minute reperfusion. The Na(+)-H(+) exchange inhibitor further suppressed d[Na(+)](i)/dt in both control and IPC hearts with concomitant improvement of functional recovery, suggesting little contribution to the mechanism of IPC. The mitochondrial ATP-sensitive K(+) (mito K(ATP)) channel activator diazoxide (30 micromol/L) completely mimicked both [Na(+)](i) kinetics and functional recovery in IPC without any additive effects to IPC. The mito K(ATP) channel blocker 5-hydroxydecanoic acid (100 micromol/L) lost protective effect as well as the attenuation of d[Na(+)](i)/dt and [Na(+)](i) recovery induced by diazoxide. However, 5-hydroxydecanoic acid also lost IPC-induced protection, but incompletely abolished the alteration of d[Na(+)](i)/dt and the [Na(+)](i) recovery. The Na(+)/K(+)-ATPase inhibitor ouabain (200 micromol/L) did not change d[Na(+)](i)/dt in non-IPC hearts, but it abolished the IPC- or diazoxide-induced reduction of d[Na(+)](i)/dt and the [Na(+)](i) recovery, whereas IPC followed by ouabain treatment showed partial functional recovery with smaller Delta[Na(+)](i) than other ouabain groups. In conclusion, alteration of Na(+) kinetics by preserving Na(+) efflux via Na(+)/K(+)-ATPase mediated by mito K(ATP) channel activation mainly contributes to functional protection in IPC hearts. The contribution of mito K(ATP) channel-independent pathway relating to Na(+) kinetics including reduced Na(+) influx is limited in functional protection of IPC.

Type IV phosphodiesterase inhibitor suppresses insulin-dependent myocardial glucose uptake.

1. Phosphodiesterase (PDE) IV has been localized at cardiomyocytes and the coronary vasculature and modulates cAMP, but the effect of PDE IV on myocardial glucose uptake has not been demonstrated. 2. Glucose uptake in rat isolated hearts treated with the PDE IV inhibitor rolipram was measured by [31P] nuclear magnetic resonance spectroscopy. 3. Under non-stimulating conditions, glucose uptake was not significantly different between control and rolipram (1 micromol/L)-treated rat hearts, whereas enhanced uptake in insulin-stimulated conditions was significantly attenuated by rolipram. 4. Phosphodiesterase IV inhibitor negatively affects insulin-dependent myocardial glucose uptake.

Clinical value of lung uptake of iodine-123 metaiodobenzylguanidine (MIBG), a myocardial sympathetic nerve imaging agent, in patients with chronic heart failure.

This study investigated the clinical value of I-123 MIBG pulmonary accumulation and washout in patients with chronic heart failure (CHF). Nineteen patients with CHF and 15 normal volunteers (NL) were included. The uptake ratio of heart to mediastinum (H/M), that of lung fields to mediastinum (L/M), and washout rate (WR) of the heart and lung fields were calculated in anterior planar images and compared with results of echocardiography and cardiac catheterization. In the CHF group, the lung uptake in delayed images increased and lung WR was decreased, suggesting pulmonary endothelial lesions. Furthermore, there was a negative correlation between right and left lung WR and pulmonary arterial diastolic pressure (PA(D)) and pulmonary arterial systolic pressure (PA(s)) in the CHF group. Since the WR of MIBG reflected PA, it may be used as an index of severity of cardiac dysfunction.

Fluorine-18 FDG myocardial positron emission tomographic findings before and after pituitary adenoma resection in a patient with acromegalic cardiomyopathy.

Because of persistently elevated growth hormone levels, acromegaly gives rise to various changes in organs mediated by insulin-like growth factor-I. In the heart, it causes myocardial hypertrophy, and, with time, heart failure. The authors performed pituitary adenomectomy in a patient with acromegalic cardiomyopathy who had heart failure; after operation, the blood growth hormone levels decreased to within the normal range and there was a marked improvement in left ventricular function by gated blood pool scintigraphy. Pre- and postoperative fluorine-18 fluorodeoxyglucose (FDG) myocardial positron emission tomography showed increased accumulation of FDG in the myocardium before surgery, but accumulation within the normal range after operation. Myocardial glucose metabolism changed when the long-term effects of growth hormone and insulin-like growth factor-I were eliminated, and this appears to be accurately reflected by FDG positron emission tomography.

Assessment of left ventricular function by gated myocardial perfusion and gated blood-pool SPECT: can we use the same reference database?

The purpose of this study was to compare left ventricular (LV) volume and ejection fraction (LVEF) measurements obtained with electrocardiographic gated single-photon emission computed tomographic (SPECT) myocardial perfusion imaging (GS-MPI) with those obtained with gated SPECT cardiac blood-pool imaging (GS-pool). Fifteen patients underwent GS-MPI with technetium-99m-tetrofosmin and GS-pool with technetium-99m-erythrocyte, within a mean interval of 8 +/- 3 days. Eight patients had suspected dilated cardiomyopathy and seven patients had angiographically significant coronary artery disease. End-diastolic volume (EDV), end-systolic volume (ESV) and LVEF measurements were estimated from GS-MPI images by means of Cedars-Sinai automatic quantitative program and from GS-pool images by the threshold technique. Mean differences between GS-MPI and GS-pool in EDV, ESV and LVEF measurements were -2.8 +/- 10.5 ml [95% confidence interval (CI): -8.6 +/- 3.0 ml], 2.6 +/- 7.3 ml (CI: -1.4 +/- 6.6 ml) and -2.3 +/- 5.1% (CI: -5.1 +/- 0.6%), respectively. No significant difference in the mean differences from 0 was found for EDV, ESV or LVEF measurements. Bland-Altman plots revealed no trend over the measured LV volumes and LVEF. For all parameters, regression lines approximated lines of identity. The excellent agreement between GS-MPI and GS-pool measurements suggests that, for estimation of LV volumes and LVEF, these two techniques may be used interchangeably and measurements by one method can serve as a reference for the other.

Detection of coronary artery disease by iodine-123-labeled iodophenyl-9-methyl pentadecanoic acid SPECT: comparison with thallium-201 and iodine-123 BMIPP SPECT.

To evaluate the ability to detect coronary artery disease (CAD) with a new iodine-123 labeled branched fatty acid analog, iodophenyl-9-methyl pentadecanoic acid (9MPA), we performed 9MPA, iodine-123 BMIPP and thallium-201 SPECT in patients with CAD. Twenty-four patients (11 with effort angina and 13 with myocardial infarction) were studied. In all patients, 9MPA SPECT was obtained at 15 min after injection. Twenty-three patients underwent stress-redistribution 201Tl SPECT and 9 patients also underwent BMIPP myocardial fatty acid imaging. The regional uptakes of 9MPA, BMIPP and 201Tl were scored semiquantitatively and the segmental agreements were compared among them. In the segment-to-segment comparison, 9MPA showed reduced activity in comparison to stress-redistribution 201Tl imaging. The defect score of 9MPA was significantly greater than that of redistribution 201Tl images (p < 0.001). In addition, segmental 9MPA uptake was lower than BMIPP and its defect score was significantly greater than that of BMIPP (p < 0.05). When coronary angiography was used as the criterion, 9MPA showed higher sensitivity and lower specificity than stress-redistribution 201Tl (p < 0.01). In conclusion, fatty acid metabolic imaging with 9MPA is a sensitive but nonspecific detector of CAD.

Characteristics of myocardial 18F-fluorodeoxyglucose positron emission computed tomography in dilated cardiomyopathy and ischemic cardiomyopathy.

Myocardial 18F-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) has been used to assess myocardial ischemia and viability, but few studies have conducted on FDG-PET for dilated cardiomyopathy (DCM). We investigated myocardial FDG uptake in patients with DCM in comparison with ischemic cardiomyopathy (ICM). Twenty-four patients with heart failure were included in this study. Fourteen of them were diagnosed as DCM and the other 10 were ICM. All of them underwent myocardial FDG-PET at fasting and after glucose loading the same day. FDG uptake was quantified by the ratio of the counts at the heart to those at the liver (H/L ratio). Left ventricular (LV) function was measured by echocardiography. We classified FDG distribution patterns in the myocardium in the fasting state into 3 types (faint uptake, regional uptake and diffuse uptake). In DCM patients, 5 had faint uptake, 7 had regional uptake, and the other 2 had diffuse uptake. On the other hand, all ICM patient had regional uptake (p < 0.05). In DCM, there were no significant relationships between the patterns and LV functions. On the other hand, there were close correlation between the H/L ratio after glucose loading and the left ventricular ejection fraction (r = 0.680, p < 0.01). The changes in PET images caused by glucose loading were classified into 2 types (non-reversing and reversing patterns). DCM significantly showed a non-reversing pattern (86%, 12 of 14 patients) whereas ICM showed mainly a reversing pattern (70%, 7 of 10 patients; p < 0.05). In conclusion, myocardial FDG uptake after glucose loading may indicate a myocardial viable mass although FDG uptake at fasting was not evidently related to LV function. The change in the pattern of the FDG image from fasting to glucose loading may be useful in differentiating DCM from ICM.

Relation between thallium-201/iodine 123-BMIPP subtraction and fluorine 18 deoxyglucose polar maps in patients with hypertrophic cardiomyopathy.

BACKGROUND: Clinical studies have shown discrepancies in the distribution of thallium-201 and iodine 123-beta-methyl-iodophenylpentadecanoic acid (BMIPP) in patients with hypertrophic cardiomyopathy (HCM). Myocardial uptake of fluorine 18 deoxyglucose (FDG) is increased in the hypertrophic area in HCM. METHODS AND RESULTS: We examined whether the distribution of a Tl-201/BMIPP subtraction polar map correlates with that of an FDG polar map. We normalized to maximum count each Tl-201 and BMIPP bull's-eye polar map of 6 volunteers and obtained a standard Tl-201/BMIPP subtraction polar map by subtracting a normalized BMIPP bull's-eye polar map from a normalized Tl-201 bull's-eye polar map. The Tl-201/BMIPP subtraction polar map was then applied to 8 patients with HCM (mean age 65+/-12 years) to evaluate the discrepancy between Tl-201 and BMIPP distribution. We compared the Tl-201/BMIPP subtraction polar map with an FDG polar map. In patients with HCM, the Tl-201/BMIPP subtraction polar map showed a focal uptake pattern in the hypertrophic area similar to that of the FDG polar map. By quantitative analysis, the severity score of the Tl-201/BMIPP subtraction polar map was significantly correlated with the percent dose uptake of the FDG polar map. CONCLUSION: These results suggest that this new quantitative method may be an alternative to FDG positron emission tomography for the routine evaluation of HCM.

Left ventricular volumes and ejection fraction calculated from quantitative electrocardiographic-gated 99mTc-tetrofosmin myocardial SPECT.

UNLABELLED: We compared the left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (LVEF) as calculated by Cedars automated quantitative gated SPECT (QGS) to those determined by first-pass radionuclide angiography (FPRNA) and contrast left ventriculography (LVG) in a group of 21 patients (mean age 61.4 +/- 9.2 y). METHODS: A total of 740 MBq 99mTc-tetrofosmin was administered rapidly into the right cubital vein at rest, and FPRNA was performed using a multicrystal gamma camera. One hour after injection, QGS was performed with a temporal resolution of 10 frames per R-R interval. LVG was performed within 2 wk. RESULTS: The EDV, ESV and LVEF calculated by QGS were highly reproducible (intraobserver, r = 0.99, r = 0.99 and r = 0.99, respectively; interobserver, r = 0.99, r = 0.99 and r = 0.99, respectively; P < 0.01) and were more consistent than those determined by FPRNA (intraobserver, r = 0.97, r = 0.95 and r = 0.93, respectively; interobserver, r = 0.86, r = 0.96 and r = 0.91, respectively; P < 0.01). There was a good correlation between EDV, ESV and LVEF by FPRNA and those by LVG (r = 0.61, r = 0.72 and r = 0.91, respectively; P < 0.01), and there was an excellent correlation between QGS and LVG (r = 0.73, r = 0.83 and r = 0.87, respectively; P < 0.01). The mean EDV by QGS (100 +/- 11.3 mL) was significantly lower than by FPRNA (132 +/- 16.8 mL) or LVG (130 +/- 8.1 mL), and the mean ESV by QGS (53.8 +/- 9.3 mL) was lower than by FPRNA (73.0 +/- 13.3 mL). Ejection fraction values were highest by LVG (57.1% +/- 3.2%), then QGS (51.8% +/- 3.0%) and FPRNA (48.9% +/- 2.4%). CONCLUSION: QGS gave more reproducible results than FPRNA. LV volumes and LVEF calculated by QGS correlated well to those by LVG.

Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury.

To elucidate the role of intracellular Na+ kinetics during ischemia and reperfusion in postischemic contractile dysfunction, intracellular Na+ concentration ([Na+]i) was measured in isolated perfused rat hearts using 23Na nuclear magnetic resonance spectroscopy. The extension of the ischemic period from 9 minutes to 15, 21, and 27 minutes (at 37 degrees C) increased [Na+]i at the end of ischemia from 270.0+/-10.4% of preischemic level (mean+/-SE, n=5) to 348.4+/-12.0% (n=5), 491.0+/-34.0% (n=7), and 505.3+/-12.1% (n=5), respectively, whereas the recovery of developed pressure worsened with the prolongation of the ischemic period (95.1+/-4.2%, 84.3+/-1. 2%, 52.8+/-13.7%, and 16.9+/-6.4% of preischemic level). The kinetics of [Na+]i recovery during reperfusion was analyzed by the fitting of a monoexponential function. When the hearts were reperfused with low-[Ca]o (0.15 mmol/L) solution, the time constants of the recovery (tau) after 15-minute (8.07+/-0.85 minutes, n=5) and 21-minute ischemia (6.44+/-0.90, n=5) were significantly extended, with better functional recovery (98.5+/-1.4% for 15-minute [P<0.05]; 98.0+/-1.0% for 21-minute [P<0.05]) compared with standard reperfusion ([Ca]o=2.0 mmol/L, tau=3.58+/-0.28 minutes for 15-minute [P<0.0001]; tau=3.02+/-0.20 for 21-minute [P<0.0001]). A selective inhibitor of Na+/Ca2+ exchanger also decelerated the [Na+]i recovery, which suggests that the recovery reflects the Na+/Ca2+ exchange activity. In contrast, high-[Ca]o reperfusion (5 mmol/L) accelerated the [Na+]i recovery after 9-minute ischemia (tau=2.48+/-0.11 minute, n=5 [P<0.0001]) and 15-minute ischemia (tau=2.10+/-0.07, n=6 [P<0. 05]), but functional recovery deteriorated only in the hearts with 15-minute ischemia (29.8+/-9.4% [P<0.05]). [Na+]i recovery after 27-minute ischemia was incomplete and decelerated by low-[Ca]o reperfusion, with limited improvement of functional recovery (42. 5+/-7.9%, n=5 [P<0.05]). These results indicate that intracellular Na+ accumulation during ischemia is the substrate for reperfusion injury and that the [Na+]i kinetics during reperfusion, which is coupled with Ca2+ influx, also determines the degree of injury.

Exercise-induced stunning continues for at least one hour: evaluation with quantitative gated single-photon emission tomography.

To elucidate the after-effect of exercise on left ventricular (LV) function, end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (LVEF) were evaluated at 1 h after exercise and at rest by technetium-99m tetrofosmin gated myocardial single-photon emission tomography (SPET) using an automated program in 53 subjects. The subjects were grouped as follows: normal scan (n = 16), ischaemia (n = 19) and infarction (n = 18), based on the interpretation of perfusion images. Postexercise LVEF did not differ from resting LVEF in the groups with normal scan and infarction. In patients with ischaemia, postexercise EDV (90+/-17 ml, mean +/-SD) and ESV (44+/-15 ml) were significantly higher than EDV (84+/-15 ml, P = 0.001) and ESV (36+/-14 ml, P<0.0005) at rest. LVEF was significantly depressed 1 h after exercise (53%+/-9% vs 58%+/-9%, P<0.0001). In ischaemic patients with depressed postexercise LVEF, LVEF difference between rest and postexercise showed a significant correlation with the sum of defect scores, which were reversible from exercise to rest perfusion images (r = 0.92, P<0.0001). These results indicate that exercise-induced LV dysfunction (myocardial stunning) continues for at least 1 h in ischaemic patients and that the extent of LVEF depression is determined by the severity of ischaemia.

Peripheral primitive neuroectodermal tumor of the ovary confirmed by CD99 immunostaining, karyotypic analysis, and RT-PCR for EWS/FLI-1 chimeric mRNA.

We report a case of peripheral primitive neuroectodermal tumor (pPNET), which belongs to the PNET/Ewing's sarcoma family, arising in the left ovary of a 29-year-old woman. Microscopically, the tumor was composed of solid nests and sheets of monotonous, primitive, small round cells with a few rosettes, making it difficult to distinguish from small cell carcinoma of the ovary. Immunohistochemically, the tumor cells showed intense cell-membranous immunoreactivity for MIC2 protein (CD99). A short-term cell culture and karyotypic analysis revealed the tumor to possess a balanced t(11;22)(q24;q12) chromosomal translocation that is highly specific for tumors of the PNET/Ewing's sarcoma family. In addition, EWS/FLI-1 chimeric mRNA that originated from the characteristic chromosomal translocation was detected by reverse transcription-polymerase chain reaction. These results confirmed the diagnostic validity of the present tumor being a pPNET, thus raising the possibility that in the past, pPNETs which have arisen in the ovary may have been mistakenly diagnosed as small cell carcinomas of the ovary.

Molecular staging of prostate cancer: comparison of nested reverse transcription polymerase chain reaction assay using prostate specific antigen versus prostate specific membrane antigen as primer.

BACKGROUND: We examined the utility for prostate cancer staging of nested reverse transcription polymerase chain reaction (RT-PCR) using either prostate specific antigen (PSA) or prostate specific membrane antigen (PSM) as primer. METHODS: LNCaP cells were used for the in vitro quantification of RT-PCR. RT-PCR was performed on the peripheral blood of 105 control subjects and 63 patients with prostate cancer (32 who eventually underwent radical prostatectomy and 31 with clinical stage D2 cancer). RESULTS: The nested RT-PCR for the PSA and PSM primers was able to detect 1 LNCaP cell per 10(6) leukemia (K562) cells. None of the control subjects was found positive for the presence of prostate cancer cells by nested RT-PCR. In the 32-patient surgery group, the results of nested RT-PCR were significantly correlated with the pathologic stage of the cancer when using PSM primers (P=2.00 x 10(-3) by Kendall's correlation test) but not when using PSA primers (P=0.06). Extraprostatic extension was significantly more closely correlated with positive PSM nested RT-PCR results (P=0.012 by Fisher's exact probability test) than with positive results of PSA, nested RT-PCR, digital rectal examination, CT imaging, level of serum PSA or Gleason score. In the untreated stage D2 patients, the positive result rate of PSM nested RT-PCR was significantly higher than that of PSA nested RT-PCR (P=0.025 by McNemar test). CONCLUSION: Nested RT-PCR using PSM primers appears to predict the prostate cancer stage more accurately than does nested RT-PCR using PSA primers or conventional clinical staging modalities.

Incorporation of two anthraquinonylmethyl groups into the 2'-O-positions of oligonucleotides: increased affinity and sequence specificity of anthraquinone-modified oligonucleotides in hybrid formation with DNA and RNA.

Oligonucleotide 15-mers containing one or two anthraquinonylmethyl groups at specified sugar residues have been prepared on an automated DNA/RNA synthesizer by using 5'-O-dimethoxytrityl 2'-O-(2-anthraquinonylmethyl)uridine 3'-O-(2-cyanoethyl)-N, N-diisopropylphosphoramidite. The purification of the modified oligonucleotides was done with denaturing polyacrylamide gel electrophoresis. The base compositions and the presence of anthraquinone group(s) in the oligonucleotides were verified with enzymatic digestion (snake venom phosphodiesterase and alkaline phosphatase) analysis and UV-vis spectral measurements. The UV melting behaviors indicate that all the oligonucleotides with anthraquinone group(s) can bind to both their complementary DNA and RNA in a manner similar to that of the unmodified oligonucleotide. All the oligonucleotides possessing anthraquinone group(s) have higher affinity for both DNA and RNA segments when compared with the unmodified oligonucleotide. The oligomer containing two anthraquinone substituents at sites separated by four nucleotides instead of six exhibits the highest affinity for both the complementary DNA and RNA. The stabilizing effect can be translated into a free energy cost of 7.1 kcal/mol for the DNA hybrid and 3.6 kcal/mol for RNA. It has been shown through mismatch/Tm studies that modification of the oligonucleotide by anthraquinone groups does not alter the sequence specificity in binding to a RNA segment.

Separation of naphthalene and flavone derivatives by micellar electrokinetic chromatography with double- and triple-chain surfactants.

Three surfactants, p-bis(2-dodecyloxymethyl-3-oxa-6-sodiosulfonatohexyloxy)benz ene (BDSB) having two sulfonate groups and two lipophilic chains, disodium 10-dodecanoyl-5,15-bis(dodecyloxymethyl)-10-aza-4,7,13,16-tetra oxa-1,19-nonadecanedisulfonate (DDBTN) having two sulfonate groups and three lipophilic chains and disodium 4,11-bis(dodecyloxymethyl)-3,6,9,12-tetraoxa-1,14-tetrade canedionate (DBTT) having two carboxylate groups and two lipophilic chains, were used in micellar electrokinetic chromatography (MEKC). Eight naphthalene derivatives were baseline separated at 10 mM BDSB or 5 mM DBTT, and five flavone derivatives at 5 mM BDSB, DDBTN or DBTT. The elution order of the naphthalene derivatives in MEKC with BDSB was identical with that with DDBTN. However, this elution order was different from that found with DBTT. In the case of the flavone derivatives, BDSB, DDBTN and DBTT produced the identical elution order. These double- and triple-chain surfactants exhibited different selectivity when compared with widely used sodium dodecyl sulfate.

Interaction of oligonucleotides containing anthraquinone at the 2'-sugar position with complementary nucleic acids.

Oligonucleotide 15-mers containing 2-anthraquinonylmethyl substituents at the different 2'-sugar residues have been synthesized. These oligomers exhibit increased stability in formation of hybrids with complementary DNA and RNA without loss of sequence specificity.