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Qun Chen

Publications and source records attributed to Qun Chen.

At least 55 records · Page 3Linked to original sources
PubMed2004

Impact of lung volume on MR signal intensity changes of the lung parenchyma.

PURPOSE: To test the hypothesis that, in magnetic resonance (MR) imaging of healthy individuals, equal relative changes in lung volume cause equal relative changes in MR signal intensity of the lung parenchyma. MATERIALS AND METHODS: In two experimental runs, 10 volunteers underwent spirometrically monitored MR imaging of the lungs, with MR images acquired at 10 incremental lung volumes ranging from total lung capacity to 10% above residual volume. Average signal intensity, signal variability, and signal intensity integrals were calculated for each volunteer and for each lung volume. The effect of lung volume on signal intensity was quantified using linear regression analysis complemented by the runs test. Slopes and intercepts of regression lines were compared with an analysis of covariance. Slopes of the lines of best fit for lung volumes and signal intensities from the two runs were compared to the slope of the line of identity. Comparisons between the two runs were visualized using Bland and Altman plots. RESULTS: The slopes of the 10 individual regression lines yielded no significant differences (F = 1.703, P = 0.101; F = 1.321, P = 0.239). The common slopes were -0.556 +/- 0.027 (P = 0.0001) for the first and -0.597 +/- 0.0031 (P = 0.0001) for the second experimental run. Both slopes displayed no significant nonlinearity (P = 0.419 and P = 0.067). There was a strong association between changes in lung volumes (rs = 0.991, P = 0.0001) and changes in signal intensity (rs = 0.889, P = 0.0001) in the two experimental runs. Lines of best fit for lung volume and signal intensities were not significantly different from the slope of the line of identity (P = 0.321 and P = 0.212, respectively). CONCLUSION: Equal changes in lung volume cause equal changes in MR signal intensity of the lung parenchyma. This linear and reproducible phenomenon could be helpful in comparing pulmonary MR signal intensity between individuals.

Adult↗
PubMed2004

Flow artifacts in steady-state free precession cine imaging.

Steady-state free precession (SSFP) cardiac cine images are frequently corrupted by dark flow artifacts, which can usually be eliminated by reshimming and retuning the scanner. A theoretical explanation for these artifacts is provided in terms of spins moving through an off-resonant point in the magnetic field, and the theory is validated using phantom experiments. The artifacts can be reproduced in vivo by detuning the center frequency by an amount in the range of half the inverse repetition time (TR). Since this offset is similar in magnitude to the frequency difference between the water and lipid peaks, a likely cause of the artifacts in vivo is that the center frequency is tuned incorrectly to the lipid peak rather than the water peak.

Artifacts↗
PubMed2004

Rapid and sensitive immunomagnetic-electrochemiluminescent detection of p53 antibodies in human serum.

The mutation of tumor suppressor p53 gene is common in malignant tumor. p53 antibodies are products of immunoresponse against abnormal p53 protein. It has been found that p53 antibodies are of importance in tumor's diagnosis, prognosis and relapse monitoring. However, current method for detecting p53 antibodies, i.e. enzyme-linked immunosorbent assay (ELISA), requires a long time with multiple steps, and the assay is only semi-quantitative. In this work, a protocol for quantitative detection of p53 antibodies in human serum using immunomagnetic electrochemiluminescence (IM-ECL) was devoloped. The immunoassay format consisted of a three antibody sandwich in which a biotinylated capture antibody, was banded with the commercial p53 protein. A detector antibody was added to bind the p53 protein at another site. Then, secondary antibody, labeled with ruthenium(II) tris-bipyridal, was added and, when bound to the bead immunocompiex, generated light in the presence of an excess of tripropylamine. The light was detected and measured by the analyzer made by us. Our experimental results indicate that the sensitivity of this assay was 10 pg of p53 antibodies per ml of reference serum (normal human serum). A stable calibration curve with a wide dynamic range was established. The calibration curve was linear from 0.01 to 1000 ng/ml, thus, making quantitation possible. An immunologic prozone effect was observed above 1000 ng p53 antibodies per milliliter of serum. Serum samples from lung and nasopharyngeal carcinoma patients were tested using the IM-ECL assay. The positive rate of p53 antibodies were 28.6% in lung carcinoma and 8.33% in nasopharyngeal carcinoma, respectively. p53 antibody concentration in the carcerous human sera were quantified from the calibration curve. In the case of lung carcinoma, a trend was found that a higher p53 antibody concentration in the serum was likely linked to a higher stage of the cancer. This trend was not found in nasopharyngeal carcinoma. The assay uses only 50 microl of sample per test and requires a 30-min incubation period in addition to a 50 s acquisition time. This assay has several advantages over the commonly used ELISA method in terms of sensitivity, linear range, and assay time. Results of the study suggest that IM-ECL is a feasible method for rapid and sensitive detection of p53 antibodies in human serum.

Antibodies↗
PubMed2004

Dark flow artifacts with steady-state free precession cine MR technique: causes and implications for cardiac MR imaging.

Steady-state free precession cine images from cardiac magnetic resonance imaging studies of 24 patients were reviewed retrospectively to identify dark flow artifacts. The cause and features of the artifacts were studied in flow phantom experiments. Dark flow artifacts were recognized in eight of the 24 cases and were characterized by low or inhomogeneous signal intensity in blood pools with little change in adjacent tissues. The artifacts could be mimicked in flow phantom experiments by deliberately deshimming the gradients and appeared periodically during imaging with off-centered frequencies. These artifacts appeared to be caused by spins moving within an inhomogeneous magnetic field.

Adult↗
PubMed2004

On improving temporal and spatial resolution of 3D contrast-enhanced body MR angiography with parallel imaging.

Use of a parallel imaging technique to improve temporal and spatial resolution at three-dimensional contrast-enhanced magnetic resonance (MR) angiography was investigated. Thirty experiments were performed in five groups of healthy subjects. In groups 1-3, the technique was used to improve imaging speed by a factor of two or four while maintaining spatial resolution. Contrast agent concentration was two to four times higher than at standard MR angiography, to take advantage of the faster imaging speed. In groups 4 and 5, the technique was used to double spatial resolution in the phase-encoding direction while maintaining imaging speed and contrast agent concentration. At a two to four times faster imaging speed, signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) almost equaled those at standard MR angiography, likely a result of increased contrast agent concentration. The use of parallel imaging to achieve higher spatial resolution was also proved feasible, but with substantial reduction in SNR and CNR.

Adult↗
PubMed2004

Effects of Pd-bacteriopheophorbide (TOOKAD)-mediated photodynamic therapy on canine prostate pretreated with ionizing radiation.

The aim of this study was to evaluate the effects of photodynamic therapy (PDT) using a novel palladium bacteriopherophorbide photosensitizer TOOKAD (WST09) on canine prostate that had been pretreated with ionizing radiation. To produce a physiological and anatomical environment in canine prostate similar to that in patients for whom radiotherapy has failed, canine prostates (n = 4) were exposed to ionizing radiation (54 Gy) 5 to 6 months prior to interstitial TOOKAD-mediated PDT. Light irradiation (763 nm, 50-200 J/cm at 150 mW/cm from a 1-cm cylindrical diffusing fiber) was delivered during intravenous infusion of TOOKAD at 2 mg/kg over 10 min. Interstitial measurements of tissue oxygen profile (pO(2)) and of local light fluence rate were also measured. The prostates were harvested for histological examination 1 week after PDT. The baseline pO(2) of preirradiated prostate was in the range 10-44 mmHg. The changes in relative light fluence rate during PDT ranged from 12 to 43%. The acute lesions were characterized by hemorrhagic necrosis, clearly distinguishable from the radiotherapy-induced pre-existing fibrosis. The lesion size was correlated with light fluence and comparable to that in unirradiated prostate treated with a similar TOOKAD-PDT protocol. There was no noticeable damage to the urethra, bladder or adjacent colon. The preliminary results obtained from a small number of animals indicate that TOOKAD-PDT can effectively ablate prostate pretreated with ionizing radiation, and so it may provide an alternative modality for those prostate cancer patients for whom radiotherapy has failed.

Animals↗
PubMed2003

Cardiotonic drugs differentially alter cytosolic [Ca2+] to left ventricular relationships before and after ischemia in isolated guinea pig hearts.

OBJECTIVE: Cardiotonic agents may differentially alter indices of the cytosolic [Ca2+]/left ventricular pressure (LVP) relationship when given before and after ischemia. We measured and calculated systolic-diastolic [Ca2+], systolic-diastolic LVP, velocity ratios (VRs) d[Ca2+]/dtmax to dLVP/dtmax (VRmax), d[Ca2+]/dtmin to dLVP/dtmin (VRmin), and area ratio (AR, area Ca2+]/area LVP per beat) before and after 30 min global ischemia in guinea pig hearts. METHODS: Hearts were perfused with levosimendan, dobutamine, dopamine, or digoxin. Ca2+ transients were recorded by indo-1 fluorescence via a fiber optic probe placed on the LV free wall. [Ca2+]/LVP loops were acquired by plotting LVP time as a function of [Ca2+] at multiple time points during the cardiac cycle. RESULTS: Ischemia reperfusion increased [Ca2+] and decreased contractility and relaxation and produced a flatter and broader [Ca2+]/LVP loop. All drugs shifted the [Ca2+]/LVP loop rightward and upward when given before and after ischemia. Dobutamine increased [Ca2+] and contractility more than other drugs. Digoxin increased [Ca2+] the least but increased contractility similar to dopamine and levosimendan. Before ischemia dopamine and digoxin both decreased VRmax and VRmin, whereas dobutamine increased VRmin, but not VRmax, and levosimendan had no effect on VR. VRmax and VRmin were markedly elevated after ischemia, but again decreased with dopamine and digoxin; dobutamine again increased VRmin, but not VRmax, and levosimendan decreased both VRmax and VRmin. Before ischemia dopamine and digoxin both decreased AR, dobutamine increased AR, and levosimendan had no effect; after ischemia AR was markedly elevated but dopamine and digoxin decreased AR, dobutamine increased AR, and levosimendan decreased AR. CONCLUSION: Although each drug enhanced contractility and relaxation both before and after ischemia by increasing cytosolic [Ca2+] and Ca2+ flux, dopamine and digoxin improved, and dobutamine worsened responsiveness to Ca2+, i.e., velocity ratio and area ratio, whereas levosimendan had no net effect before ischemia but improved responsiveness after ischemia.

Animals↗
PubMed2003

Regulation of constitutive expression of mouse PTEN by the 5'-untranslated region.

PTEN tumor suppressor serves as a major negative regulator of survival signaling mediated by PI3 kinase/AKT/protein kinase B pathway, and is inactivated in various human tumors. Elucidation of mechanisms responsible for PTEN expression is important for providing insight into strategies to control the loss of PTEN expression in human cancers. Although recent studies suggested that p53 and Egr-1 can modulate induced PTEN expression, the mechanism responsible for ubiquitous constitutive expression of PTEN remains elusive. PTEN mRNA contains a highly conserved and GC-rich 5'-untranslated region (5'-UTR). Recently, it has been shown that the long 5'-UTR sequences of several growth-regulated mRNAs contain promoters that can generate mRNAs with shorter 5'-UTRs. In this paper, we tested whether the 5'-UTR sequence of mouse PTEN contains a promoter that is responsible for constitutive expression of PTEN. We found that the long 5'-UTR sequence of mouse PTEN severely inhibits translation of PTEN and a heterologous gene firefly luciferase. Deletion of the most 5'-UTR sequence would enhance translation efficiency 100-fold. We also showed that the 5'-UTR sequence of mouse PTEN does not have an internal ribosome entry site (IRES) that can mediate cap-independent initiation of translation. Instead, we found that the 5'-UTR sequence of mouse PTEN contains a strong promoter that drives the production of a transcript with shorter 5'-UTRs, which can be translated with higher efficiency. This promoter was mapped to the region between -551 and -220 bases upstream of the translation start codon. Cotransfection analysis using Drosophila SL2 cells showed that Sp1 is one of the major transcription factors that can constitutively activate this promoter. Two endogenous PTEN transcripts with 5'-UTRs of 193 and 109 bases were found in DU145 and H226 cell lines. Based on these observations, we conclude that the PTEN expression may be regulated at both transcriptional and translational levels, and that the 5'-UTR sequence of PTEN contains a promoter that is responsible for constitutive PTEN expression.

5' Untranslated Regions↗
PubMed2003

Production of reactive oxygen species by mitochondria: central role of complex III.

The mitochondrial respiratory chain is a major source of reactive oxygen species (ROS) under pathological conditions including myocardial ischemia and reperfusion. Limitation of electron transport by the inhibitor rotenone immediately before ischemia decreases the production of ROS in cardiac myocytes and reduces damage to mitochondria. We asked if ROS generation by intact mitochondria during the oxidation of complex I substrates (glutamate, pyruvate/malate) occurred from complex I or III. ROS production by mitochondria of Sprague-Dawley rat hearts and corresponding submitochondrial particles was studied. ROS were measured as H2O2 using the amplex red assay. In mitochondria oxidizing complex I substrates, rotenone inhibition did not increase H2O2. Oxidation of complex I or II substrates in the presence of antimycin A markedly increased H2O2. Rotenone prevented antimycin A-induced H2O2 production in mitochondria with complex I substrates but not with complex II substrates. Catalase scavenged H2O2. In contrast to intact mitochondria, blockade of complex I with rotenone markedly increased H2O2 production from submitochondrial particles oxidizing the complex I substrate NADH. ROS are produced from complex I by the NADH dehydrogenase located in the matrix side of the inner membrane and are dissipated in mitochondria by matrix antioxidant defense. However, in submitochondrial particles devoid of antioxidant defense ROS from complex I are available for detection. In mitochondria, complex III is the principal site for ROS generation during the oxidation of complex I substrates, and rotenone protects by limiting electron flow into complex III.

Animals↗
PubMed2003

Computing oxygen-enhanced ventilation maps using correlation analysis.

Correlation maps of oxygen-enhanced ventilation were obtained in nine healthy volunteers using complete and selected image series. The complete series included all images acquired with the subjects alternately inhaling room air and 100% oxygen. The selected series were the subsets of the complete series and included only co-registered images that showed matched diaphragmatic position at maximal expiration. Cross-correlation was computed between the time response function of each pixel and the input function representing the alternation between periods of room air and 100% oxygen inhalation. The confidence level for the correlation analysis was set to 0.01. Pulmonary parenchymal anatomy was consistently reproduced throughout the lung, even in anterior slices where published data have reported correlation problems. The overall average correlation coefficient was 0.66 +/- 0.07 for the complete series and 0.75 +/- 0.08 for the selected series. It was concluded that correlation analysis could be used to reconstruct qualitative oxygen-enhanced ventilation maps.

Adult↗
PubMed2003

Effect of low [CaCl2] and high [MgCl2] cardioplegia and moderate hypothermic ischemia on myoplasmic [Ca2+] and cardiac function in intact hearts.

OBJECTIVE: Cold cardioplegia (CP) protects against ischemic damage in part by reducing [Ca(2+)](i) overload on reperfusion. Hyperkalemic cardioplegic solutions are widely used in coronary artery bypass procedures, and the specific ionic composition of these solutions may contribute to their variable myocardial protective effects secondary to reduced Ca(2+)(i) loading. We reported previously that CP decreased the rise in cardiac diastolic (dia) [Ca(2+)](i) observed during 4 h cold storage at 3 degrees C in Krebs-Ringer's (KR) solution and decreased dia[Ca(2+)](i) and increased systolic (sys) [Ca(2+)](i) and function on reperfusion after cold storage. Our aim here was to determine if low Ca(2+)(o) and high Mg(2+)(o) adds to the protective effects of high K(+)(o) by decreasing [Ca(2+)](i) during ischemia and reperfusion. METHODS: We compared effects of 4.5 mM K(+)(o), 2.5 mM Ca(2+)(o) and 2.4 mM Mg(2+)(o) KR solution with a higher K(+)(o) (18 mM), a lower Ca(2+)(o) (1.25 mM) and/or higher Mg(2+)(o) (7.2 mM) CP solutions on cardiac mechanic function and sys and dia[Ca(2+)](i) during and after moderate hypothermic global ischemia (17 degrees C for 4 h) in guinea pig intact hearts isolated by the Langendorff technique. Isovolumetric left ventricular pressure (LVP) was measured with a transducer connected to a fluid-filled balloon placed in the LV and [Ca(2+)](i) was measured using indo-1 fluorescence and a fiberoptic cable placed on the LV free wall. RESULTS: For all CP groups compared to the KR control group after 60 min reperfusion, we observed significant lowering of dia[Ca(2+)](i) by 47%, left ventricular diastolic pressure (diaLVP) by 55%, and infarct size by 43%. We also found significant elevation of sys[Ca(2+)](i) by 25%, d[Ca(2+)](i)/dt(max) and d[Ca(2+)](i)/dt(min) by 33 and 34%, sys-diaLVP by 55%, dLVP/dt(max) and dLVP/dt(min) by 34 and 40%, coronary flow by 31%, cardiac efficiency by 21%, and MVO(2) by 25%. These results indicate that CP reduces myoplasmic Ca(2+) loading and improves mechanical and metabolic function on warm reperfusion compared to KR. However, there were no differences in these indices of Ca(2+)(i) cardiac function or metabolism among any CP group after warm reperfusion with KR solution. CONCLUSION: Increasing K(+)(o) to produce cardiac arrest was the most cardioprotective effect of CP against ischemia reperfusion injury; lowering Ca(2+)(o) or raising Mg(2+)(o) did not add to this protective effect or additionally alter [Ca(2+)](i).

Animals↗
PubMed2003

Effects and mechanisms of glucosides of chaenomeles speciosa on collagen-induced arthritis in rats.

Effects of glucosides of chaenomeles speciosa (GCS)-a Chinese traditional herbal medicine (CTM) on inflammatory and immune responses and its mechanisms in collagen-induced arthritis (CIA) rat were studied. Hind paw volumes of rats were measured by volume meter; lymphocyte proliferation, interleukin-1, interleukin-2, TNF-alpha level was determined by 3-(4,5-2 dimethylthiazal-2yl)2,5-diphenyltetrazoliumbromide (MTT) assay; cAMP level in synoviocytes was analyzed by competitive protein binding assay (CPBA). mRNA expression of G(i,), G(s), and TNF-alpha of synoviocytes in CIA rats was measured by RT-PCR and antibodies to collagen type II (CII) were determined by enzyme-linked immunosorbent assay (ELISA), respectively. There was a marked secondary inflammatory response in CIA model, which accompanied with the decrease of body weight and the weight of immune organs simultaneously. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) inhibited the inflammatory response and restored body weight and the weight of immune organs of CIA rats. Lymphocyte proliferation and IL-2 production of CIA rats increases, together with IL-1 and TNF-alpha in peritoneal macrophages and synoviocytes. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) reduced above changes significantly. GCS at the concentration of 0.5, 2.5, 12.5, 62.5, 125 mg x l(-1) increased cAMP level of synoviocytes, which decreased in CIA rats in vitro. At the same time, GCS inhibited mRNA expression of G(i,) and TNF-alpha of synoviocytes and increased mRNA expression of G(s) of synoviocytes in CIA rats. GCS had no effect on the concentration of antibodies to CII. GCS possesses anti-inflammatory and immunoregulatory actions and has a therapeutic effect on CIA rats due to G protein-AC-cAMP transmembrane signal transduction of synoviocytes, which play a crucial role in pathogenesis of this disease.

Animals↗
PubMed2003

Preconditioning with sevoflurane reduces changes in nicotinamide adenine dinucleotide during ischemia-reperfusion in isolated hearts: reversal by 5-hydroxydecanoic acid.

BACKGROUND: Ischemia causes an imbalance in mitochondrial metabolism and accumulation of nicotinamide adenine dinucleotide (NADH). We showed that anesthetic preconditioning (APC), like ischemic preconditioning, improved mitochondrial NADH energy balance during ischemia and improved function and reduced infarct size on reperfusion. Opening adenosine triphosphate-sensitive potassium (K(atp)) channels may be involved in triggering APC. The authors tested if effects of APC on NADH concentrations before, during, and after ischemia are reversible by 5-hydroxydecanoate (5-HD), a putative mitochondrial K channel blocker. METHODS: Nicotinamide adenine dinucleotide fluorescence was measured in 60 guinea pig Langendorff-prepared hearts assigned into five groups: (1) no treatment before ischemia; (2) APC by exposure to 1.3 mm sevoflurane for 15 min; (3) 200 microm 5-HD from 5 min before to 15 min after sevoflurane exposure; (4) 35 min 5-HD alone; and (5) no treatment and no ischemia. Sevoflurane was washed out for 30 min, and 5-HD for 15 min, before 30-min ischemia and 120-min reperfusion. RESULTS: Nicotinamide adenine dinucleotide was reversibly increased during sevoflurane exposure before ischemia, and the increase and rate of decline in NADH during ischemia were reduced after APC. 5-HD abolished these changes in NADH. On reperfusion, function was improved and infarct size reduced after APC compared with other groups. CONCLUSION: Anesthetic preconditioning was evidenced by improved mitochondrial bioenergetics as assessed from NADH concentrations during ischemia and by attenuated reperfusion injury. Reversal of APC by bracketing sevoflurane exposure with 5-HD suggests that APC is triggered by mitochondrial K channel opening or, alternatively, by attenuated mitochondrial respiration without direct involvement of mitochondrial K channel opening.

ATP-Binding Cassette Transporters↗
PubMed2003

Na+/H+ exchange inhibition with cardioplegia reduces cytosolic [Ca2+] and myocardial damage after cold ischemia.

Cold cardioplegia protects against reperfusion damage. Blocking Na+/H+ exchange may be as protective as cardioplegia by improving the left ventricular pressure (LVP)-[Ca2+] relationship after cold ischemia. In guinea pig isolated hearts subjected to cold ischemia (4 h, 17 degrees C) and reperfusion, the cardioprotective effects of a Krebs-Ringer (KR) solution, a cardioplegia solution, a KR solution containing the Na+/H+ exchange inhibitor eniporide (1 microM), and a cardioplegia solution containing eniporide were compared. Treatments were given before and initially after cold ischemia. Systolic and diastolic [Ca2+] were calculated from indo-1 fluorescence transients recorded at the LV free wall. During ischemia, diastolic [Ca2+] increased in each group but more so in the KR group. Peak systolic and diastolic [Ca2+] on initial reperfusion were highest after KR and smallest after cardioplegia + eniporide. After reperfusion, systolic-diastolic LVP (% of baseline) and infarct size (%), respectively, were KR, 47 +/- 3%, 37 +/- 4%; cardioplegia, 71 +/- 5%*, 20 +/- 2.2%*; KR + eniporide, 73 +/- 5%*, 11 +/- 3%* dagger; and cardioplegia + eniporide 77 +/- 3%*, 10 +/- 1.4%* dagger (*P </= 0.05 vs KR; dagger P </= 0.05 vs cardioplegia). Ca2+ overload was reduced in each treated group, and most in the cardioplegia + eniporide group, and was associated with the improved function. Inhibition of Na+/H+ exchange was as effective as cardioplegia in restoring function and better than cardioplegia in reducing infarct size after hypothermic ischemia. The combination of cardioplegia and Na+/H+ exchange inhibition did not produce additive protective effects but caused a larger decrease in Ca2+ loading.

Animals↗
PubMed2003

How inotropic drugs alter dynamic and static indices of cyclic myoplasmic [Ca2+] to contractility relationships in intact hearts.

The authors examined effects of positive (dopamine and digoxin) and negative (nifedipine and lidocaine) inotropic interventions on the instantaneous cyclic relationship between myoplasmic [Ca2+] and simultaneously developed left ventricular pressure (LVP) in intact guinea pig hearts. Novel indices were developed to quantify this relationship based on (1) transient [Ca2+] and LVP signal morphology, ie, maxima and minima, peak derivatives, beat areas, durations, and ratios of indices of LVP to [Ca2+]; (2) temporal delay; and (3) LVP versus [Ca2+] loop morphology, ie, orientation, size, hysteresis, position, shape, and duration. These analyses were used to assess the cost of phasic [Ca2+] for contraction and relaxation over one beat after inotropic intervention. It was found that dopamine and digoxin increased contractile and relaxation responsiveness to phasic [Ca2+], cumulative Ca2+, and net Ca2+ flux. Unlike dopamine, digoxin did not decrease relaxation response time. Nifedipine and lidocaine decreased contractile and relaxation responsiveness to phasic [Ca2+], cumulative Ca2+, and net Ca2+ flux. Unlike lidocaine, nifedipine decreased net available Ca2+ and Ca2+ influx. Positive inotropic agents increased [Ca2+]-LVP loop area and hysteresis and resulted in a more vertically oriented loop. Nifedipine and lidocaine decreased these loop indices and lidocaine exhibited greater loop hysteresis than did nifedipine. These novel indices provide a quantitative assessment of myoplasmic [Ca2+] handling for cardiac contractile function.

Animals↗
PubMed2003

Hyperoxygenation enhances the tumor cell killing of photofrin-mediated photodynamic therapy.

Tumor hypoxia, either preexisting or as a result of oxygen depletion during photodynamic therapy (PDT) light irradiation, can significantly reduce the effectiveness of PDT-induced cell killing. To overcome tumor hypoxia and improve tumor cell killing, we propose using supplemental hyperoxygenation during Photofrin-PDT. The mechanism for the tumor cure enhancement of the hyperoxygenation-PDT combination is investigated using an in vivo-in vitro technique. A hypoxic tumor model was established by implanting mammary adenocarcinoma in the hind legs of mice. Light irradiation (200 J/cm2 at either 75 or 150 mW/cm2), under various oxygen supplemental conditions (room air, carbogen, 100% normobaric or hyperbaric oxygen), was delivered to animals that received 12.5 mg/kg Photofrin 24 h before light irradiation. Tumors were harvested at various time points after PDT and grown in vitro for colony formation analysis. Treated tumors were also analyzed histologically. The results show that when PDT is combined with hyperoxygenation, the hypoxic condition could be improved and the cell killing rate at various time points after PDT could be significantly enhanced over that without hyperoxygenation, suggesting an enhanced direct and indirect cell killing associated with high-concentration oxygen breathing. This study further confirms our earlier observation that when a PDT treatment is combined with hyperoxygenation it can be more effective in controlling hypoxic tumors.

Adenocarcinoma↗
PubMed2003

Effects and mechanisms of melatonin on immune responses in mice of different months.

AIM: To study the effects and mechanisms of melatonin (MT) on immune responses in mice of different months. METHODS: Thymocyte proliferation and IL-2 activity were assayed by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) and activated mouse splenocyte proliferation methods, respectively; cAMP and methionine-enkephalin (met-Enk) level was determined by competitive protein binding assay and radioimmunoassay, respectively. RESULTS: The function of lymphocytes, obtained from BALB/c mice aged 6 and 11 months were decreased, which was restored by melatonin at the dose of 5 mg/kg or 30 mg/kg. In vitro, proliferation of lymphocytes in 11-month-old mice was decreased and cAMP level was increased. Melatonin (0.1 nmol/L or 1 micromol/L) had negative regulation to this. Forskolin (10 micromol/L) enhanced the cAMP level of lymphocytes in 2- and 11-month-old mice (P<0.01), which was antagonized partially by melatonin and this effect of melatonin was also abolished by pertussis toxin (1 mg/L) completely. Melatonin (1 micromol/L and 0.1 nmol/L) increased the content of met-Enk of lymphocytes in 2- and 11-month-old mice, respectively (P<0.01), which was blocked by nifedipine (1 micromol/L). CONCLUSION: Melatonin exerted an effect on immune responses in mice of different months, which might be mediated by G protein-AC-cAMP signal transduction pathway and regulation of met-Enk level.

Adjuvants, Immunologic↗