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Qun Chen

Publications and source records attributed to Qun Chen.

At least 73 records · Page 4Linked to original sources
PubMed2003

[Analysis of mood factors in prostatitis and Molida therapy].

OBJECTIVES: To analyze the mood factors in prostatitis and evaluate the effects of Molida psychological therapy. METHODS: Two hundred and thirty-six chronic prostatitis patients were divided according to the course of disease into above 6 months group (n = 31) and below 6 months group(n = 205) as well as into sexual disease group(n = 25) and non-sexual disease group(n = 211). An investigation was made by self-rating method on the basis of the National Institutes of Health Chronic Prostatitis Symptom Index(NIH-CPSI) and Symptom Checklist 90 (SCL-90) and 56 cases were rated again after Molida therapy. RESULTS: 1. The scores of SCL-90 in 236 prostatitis patients were significantly higher than normal(P < 0.01). The factor scores of SCL-90 showed one-item positive in 107 patients (45.2%), of whom 27 (25.2%) had depressive disorder and 80(74.77%) had anxiety (23 with significant compulsion). Thirty-eight cases(16.1%) were two items positive. 2. The scores of SCL-90 were significantly higher in the > 6 months group of history and the sexual disease group than in the control group (P < 0.01). 3. The scores of NIH-CPSI showed a positive correlation with those of SCL-90 and both scores in 43/56 cases were significantly decreased after psychological treatment (P < 0.01). CONCLUSIONS: The mood factor plays an important role in aggravating symptoms in chronic prostatis patients and causes difficulty for management. Molida may significantly improve the mood and symptoms of the chronic prostatitis patient.

Adult↗
PubMed2002

Structural and functional consequences of mutating cysteine residues in the amino terminus of human multidrug resistance-associated protein 1.

Multidrug resistance-associated protein 1 (MRP1) is a member of the ATP-binding cassette membrane transport superfamily and is responsible for multidrug resistance in cancer cells. Currently, there are nine known human MRPs. Distinct from many other members of the ATP-binding cassette superfamily, human MRP1 and four other MRPs have an additional membrane-spanning domain (MSD) with a putative extracellular amino terminus. The functional significance of this additional MSD (MSD1) is currently unknown. To understand the role of MSD1 in human MRP1 structure and function, we studied the amino-terminal 33 amino acids. We found that the amino terminus of human MRP1 has two cysteine residues (Cys(7) and Cys(32)) that are conserved among the five human MRPs that have MSD1. Mutation analyses of the two cysteines in human MRP1 revealed that the Cys(7) residue is critical for the MRP1-mediated drug resistance and leukotriene C(4) transport activity. On the other hand, mutation of Cys(32) reduced only moderately the MRP1 function. The effect of Cys(7) mutation on MRP1 activity appears to be due to the 5-7-fold decrease in the maximal transport rate V(max). We also found that mutation of Cys(7) changed the amino-terminal conformation of MRP1. This conformational change is likely responsible for the decrease in V(max) of LTC(4) transport mediated by the mutant MRP1. Based on these studies, we conclude that the amino terminus of human MRP1 is important and that the Cys(7) residue plays a critical role in maintaining the proper structure and function of human MRP1.

Adenosine Triphosphate↗
PubMed2002

Cytoplasmic retraction of the amino terminus of human multidrug resistance protein 1.

Human multidrug resistance protein 1 (MRP1) is a member of the ATP-binding cassette (ABC) transport superfamily which also includes human multidrug resistance 1 (MDR1) gene product P-glycoprotein (Pgp). Overexpression of MRP1 or Pgp causes multidrug resistance in cancer cells. Different from Pgp, MRP1 contains an extra membrane-spanning domain (MSD1) with a putative extracellular amino terminus in addition to the core structure of two MSDs and two NBDs (nucleotide-binding domains). The structural and functional significance of the additional MSD1 in MRP1 remains elusive. In this study, we generated an IgG1 subclass monoclonal antibody, IU2H10, specific to the amino terminus of human MRP1 and mapped its epitope to 10 amino acids (S8ADGSDPLWD17). It can be used for Western blot, immunoprecipitation, and indirect immunofluorescence studies of human MRP1. However, surprisingly we found that IU2H10 cannot react with MRP1 unless cells are permeabilized. Furthermore, the IU2H10 epitope is exposed extracellularly when the carboxyl-terminal core domain of human MRP1 is deleted. Examination of the amino-terminal sequence of human MRP1 suggests that it consist of mainly coiled structures. These observations provide evidence for a model that is different from the prevailing extracellular location of the amino terminus of human MRP1. It is possible that part of the amino terminus of human MRP1, following exposure to the lumen of the endoplasmic reticulum, is retracted to the cytoplasm.

Amino Acid Sequence↗
PubMed2002

Humanized mice as a model for rheumatoid arthritis.

Genetic susceptibility to rheumatoid arthritis (RA), a common autoimmune disease, is associated with certain HLA-DR4 alleles. Treatments are rarely curative and are often tied to major side effects. We describe the development of a humanized mouse model wherein new, less toxic, vaccine-like treatments for RA might be pretested. This model includes four separate transgenes: HLA-DR*0401 and human CD4 molecules, a RA-related human autoantigenic protein (HCgp-39), and a T-cell receptor (TCRalphabeta) transgene specific for an important HCgp-39 epitope, eliciting strong Th1 responses in the context of HLA-DR*0401.

Animals↗
PubMed2002

Influence of oxygen flow rate on signal and T(1) changes in oxygen-enhanced ventilation imaging.

PURPOSE: To investigate the optimal oxygen flow rate for oxygen-enhanced MR ventilation imaging. MATERIALS AND METHODS: Using a cardiac-triggered nonselective inversion recovery (IR) half Fourier single-shot fast spin echo sequence, series of images were acquired with the subject alternately inhaling room air and 100% oxygen. Oxygen flow rates of 5 L/min, 10 L/min, 15 L/min, 20 L/min, and 25 L/min were studied, and signal intensity from the oxygen-enhanced ventilation images and T(1) of the lung were measured. RESULTS: The average signal intensity was 63.0 +/- 21.0 for 5 L/min, 98.7 +/- 26.8 for 10 L/min, 133.8 +/- 20.0 for 15 L/min, 138.7 +/- 19.7 for 20 L/min, and 139.2 +/- 37.9 for 25 L/min. The average T(1)'s of the lung were 1399 msec +/- 130 msec for room air, 1314 msec +/- 101 msec for 5 L/min, 1276 msec +/- 105 msec for 10 L/min, 1207 msec +/- 71 msec for 15 L/min, 1206 msec +/- 90 msec for 20 L/min, and 1207 msec +/- 42 msec for 25 L/min. CONCLUSION: The optimal flow rate is 15 L/min for oxygen-enhanced ventilation imaging.

Adult↗
PubMed2002

Ventilation-perfusion ratio of signal intensity in human lung using oxygen-enhanced and arterial spin labeling techniques.

This study investigates the distribution of ventilation-perfusion (V/Q) signal intensity (SI) ratios using oxygen-enhanced and arterial spin labeling (ASL) techniques in the lungs of 10 healthy volunteers. Ventilation and perfusion images were simultaneously acquired using the flow-sensitive alternating inversion recovery (FAIR) method as volunteers alternately inhaled room air and 100% oxygen. Images of the T(1) distribution were calculated for five volunteers for both selective (T(1f)) and nonselective (T(1)) inversion. The average T(1) was 1360 ms +/- 116 ms, and the average T(1f) was 1012 ms +/- 112 ms, yielding a difference that is statistically significant (P < 0.002). Excluding large pulmonary vessels, the average V/Q SI ratios were 0.355 +/- 0.073 for the left lung and 0.371 +/- 0.093 for the right lung, which are in agreement with the theoretical V/Q SI ratio. Plots of the V/Q SI ratio are similar to the logarithmic normal distribution obtained by multiple inert gas elimination techniques, with a range of ratios matching ventilation and perfusion. This MRI V/Q technique is completely noninvasive and does not involve ionized radiation. A limitation of this method is the nonsimultaneous acquisition of perfusion and ventilation data, with oxygen administered only for the ventilation data.

Adult↗
PubMed2002

Band artifacts due to bulk motion.

Band artifacts due to bulk motion were investigated in images acquired with fast gradient echo sequences. A simple analytical calculation shows that the width of the artifacts has a square-root dependence on the velocity of the imaged object, the time taken to acquire each line of k-space and the field of view in the phase-encoding direction. The theory furthermore predicts that the artifact width can be reduced using parallel imaging by a factor equal to the square root of the acceleration parameter. The analysis and results are presented for motion in the phase- and frequency-encoding directions and comparisons are made between sequential and centric ordering. The theory is validated in phantom experiments, in which bulk motion is simulated in a controlled and reproducible manner by rocking the scan table back and forth along the bore axis. Preliminary cardiac studies in healthy human volunteers show that dark bands may be observed in the endocardium in images acquired with nonsegmented fast gradient echo sequences. The fact that the position of the bands changes with the phase-encoding direction suggests that they may be artifacts due to motion of the heart walls during the image acquisition period.

Artifacts↗
PubMed2002

Inhibition of Na(+)/H(+) isoform-1 exchange protects hearts perfused after 6-hour cardioplegic cold storage.

OBJECTIVES: Cardiac ischemia-reperfusion activates Na(+)/H(+) exchange; excess Na(+) and the resulting Ca(2+) overload, through reverse Na(+)/Ca(2+) exchange, cause cellular injury and cardiac dysfunction. We postulated that inhibiting the Na(+)/H(+) isoform-1 exchanger would add to the protection of hearts after long-term cold storage in acidic cardioplegic solution. METHODS: Guinea pig hearts were isolated and perfused at 37 degrees C with Krebs-Ringer's solution (KRS) and then switched to an acidic St. Thomas solution (STS) at 25 degrees C. Perfusion was stopped at 10 degrees C, and hearts were stored for 6 hours in STS at 3.4 degrees C. On reperfusion to 25 degrees C, hearts were perfused with KRS for 60 minutes. Hearts were divided into 4 groups: sham control (SHAM); eniporide (EPR, EMD96785) IV, 1 mg/kg given IV over 15 minutes before heart isolation; EPR intracoronary, 1 micromol/liter in STS given intracoronary after heart isolation; and EPR IV and intracoronary. RESULTS: Values at 60 minutes reperfusion (the percentage of control [100%] before cold storage) are given, respectively, for EPR IV, EPR intracoronary, and EPR IV and intracoronary vs drug-free SHAM (SEM, *p < 0.05 vs SHAM): 72% +/- 3%*, 65% +/- 3%*, and 81% +/- 2%* vs 55% +/- 3% for left ventricular pressure; 94% +/- 3%*, 96% +/- 5%*, and 102% +/- 2%* vs 81% +/- 3% for coronary flow; 60% +/- 2%, 58% +/- 3%, and 74%* +/- 3% vs 58% +/- 4% for cardiac efficiency; 106% +/- 2%*, 108% +/- 3%*, and 107% +/- 2%* vs 116% +/- 4% for percentage of O(2) extraction. Infarct size as percentage of ventricular weight was 20% +/- 3%*, 31% +/- 3%, and 6% +/- 2%* vs 35% +/- 3% (SHAM) after 60 minutes of reperfusion. CONCLUSIONS: Na(+)/H(+) isoform-1 exchanger inhibition, particularly if given IV before storage and intracoronary during cooling and rewarming, adds to the protection of cardioplegic solutions.

Animals↗
PubMed2002

Effects and mechanisms of melatonin on inflammatory and immune responses of adjuvant arthritis rat.

AIM: To study the effects of melatonin on inflammatory and immune responses and its mechanisms. METHODS: The model of adjuvant-induced arthritis (AA) rat was induced by Freund's complete adjuvant (FCA); the thymocyte proliferation and IL-2 production were assayed by 3-(4,5-2dimethylthiazal-2yl)2,5-diphenyltetrazoliumbromide (MTT) and activated mouse splenocytes proliferation, respectively; cAMP and methionine-enkephalin (Met-Enk) level were determined by competitive protein binding assay (CPBA) and radioimmuno-assay, respectively. RESULTS: There was a marked inflammatory response in AA model, which was accompanied by the decreases of thymocyte proliferation and IL-2 production simultaneously. The prophylactic and therapeutic administration of melatonin (1, 10 and 100 microg kg(-1), ig x 7 days) inhibited the inflammatory response and enhanced thymocytes proliferation and IL-2 production significantly in AA rats. In vitro, melatonin, at the concentrations of 10(-7) and 10(-6) mol l(-1) could enhance the thymocyte proliferation in AA rats. The cAMP level stimulated by forskolin (F, a selective adenylate cyclase [AC] activator) in AA rats was higher than that in the control groups. Melatonin (10(-10) or 10(-6) mol l(-1)) had down-regulation on the above increased cAMP levels, which could be abolished by pertussis toxin (PT). Meanwhile, the decrease of thymocyte proliferation in AA rats had a marked relation with the decrease of Met-Enk level in these thymocytes, melatonin (10(-10) or 10(-6) mol l(-1)) could markedly enhance the Met-Enk level, which were blocked by nifedipine, a Ca2+ channel antagonist. CONCLUSIONS: Melatonin possesses anti-inflammatory and immunoregulatory actions, the G protein-AC-cAMP transmembrane signal and Met-Enk release in thymocyte are important mechanisms of this action.

Animals↗
PubMed2002

Anesthetic preconditioning attenuates mitochondrial Ca2+ overload during ischemia in Guinea pig intact hearts: reversal by 5-hydroxydecanoic acid.

UNLABELLED: Cardiac ischemia/reperfusion (IR) injury is associated with mitochondrial (m)Ca(2+) overload. Anesthetic preconditioning (APC) attenuates IR injury. We hypothesized that mCa(2+) overload is decreased by APC in association with mitochondrial adenosine triphosphate-sensitive K(+) (mK(ATP)) channel opening. By use of indo-1 fluorescence, m[Ca(2+)] was measured in 40 guinea pig Langendorff-prepared hearts. Control (CON) hearts received no treatment for 50 min before IR; APC hearts were exposed to 1.2 mM (8.8 vol%) sevoflurane for 15 min; APC + 5-hydroxydecanoate (5-HD) hearts received 200 micro M 5-HD from 5 min before to 15 min after sevoflurane exposure; and 5-HD hearts received 5-HD for 35 min. Sevoflurane was washed out for 30 min and 5-HD for 15 min before 30 min of global ischemia and 120 min of reperfusion. During ischemia, the peak m[Ca(2+)] accumulation was decreased by APC from 489 +/- 37 nM (CON) to 355 +/- 28 nM (P < 0.05); this was abolished by 5-HD (475 +/- 38 nM m[Ca(2+)]). APC resulted in improved function and reduced infarct size on reperfusion, which also was blocked by 5-HD. 5-HD pretreatment alone did not affect m[Ca(2+)] (470 +/- 34 nM) or IR injury. Thus, preservation of function and morphology on reperfusion is associated with attenuated mCa(2+) accumulation during ischemia. Reversal by 5-HD suggests that APC may be triggered by opening mK(ATP) channels. IMPLICATIONS: Myocardial ischemia/reperfusion injury is associated with mitochondrial Ca(2+) overload. Mitochondrial [Ca(2+)] and function were measured in guinea pig isolated hearts. Anesthetic preconditioning attenuated mitochondrial Ca(2+) overload during ischemia, improved function, and reduced infarct size. Reversal by 5-hydroxydecanoate suggests that anesthetic preconditioning may be triggered by mitochondrial adenosine triphosphate-sensitive K channel opening.

Anesthetics↗
PubMed2002

Sevoflurane preconditioning before moderate hypothermic ischemia protects against cytosolic [Ca(2+)] loading and myocardial damage in part via mitochondrial K(ATP) channels.

BACKGROUND: Brief sevoflurane exposure and washout (sevoflurane preconditioning [SPC]) before 30-min global ischemia at 37 degrees C is known to improve cardiac function, decrease cytosolic [Ca(2+)] loading, and reduce infarct size on reperfusion. It is not known if anesthetic preconditioning (APC) applies as well to hypothermic ischemia and reperfusion and if K(ATP) channels are involved. The authors examined in guinea pig isolated hearts the effect of sevoflurane exposure before 4-h global ischemia at 17 degrees C on cardiac function, cytosolic [Ca(2+)] loading, and infarct size. In addition they tested the potential role of the mitochondrial K(ATP) channel in eliciting the cardioprotection by SPC. METHODS: Hearts were randomly assigned to (1) a nontreated hypothermic ischemia group (CON), (2) a group given 3.5 vol% sevoflurane for 15 min with a 15-min washout before hypothermic ischemia (SPC), and (3) an SPC group in which anesthetic exposure was bracketed with 200 microm 5-hydroxydecanoate (5-HD) from 5 min before until 5 min after sevoflurane (SPC + 5-HD). Cytosolic [Ca(2+)] was measured in the left ventricular (LV) free wall with the intracellularly loaded fluorescence probe indo-1. RESULTS: Initial reperfusion in CON hearts markedly increased systolic and diastolic [Ca(2+)] and reduced contractility (dLVP/dt(max)), relaxation (diastolic LVP, dLVP/dt(min)), myocardial oxygen consumption (MvO(2)), and cardiac efficiency. In SPC hearts, cytosolic [Ca(2+)] overloading (especially diastolic [Ca(2+)]) was decreased with increased myocardial [Ca(2+)] influx (d[Ca(2+)]/dt(max)) and efflux (d[Ca(2+)]/dt(min)), improved contractility, relaxation, coronary flow, MvO(2), cardiac efficiency, and decreased infarct size. In SPC + 5HD hearts, the reduction in infarct size was antagonized by 5-HD, but functional return was less affected by 5-HD. CONCLUSIONS: Anesthetic preconditioning occurs after long-term hypothermic ischemia, and the infarct size reduction is the result, in part, of mitochondrial K(ATP) channel opening.

ATP-Binding Cassette Transporters↗
PubMed2002

Cardiac preconditioning with 4-h, 17 degrees C ischemia reduces [Ca(2+)](i) load and damage in part via K(ATP) channel opening.

Brief ischemia before normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear whether it protects against long-term moderate hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia before 4 h, 17 degrees C hypothermic ischemia on cardiac cytosolic [Ca(2+)], mechanical and metabolic function, and infarct size, and 2) the potential role of K(ATP) channels in eliciting cardioprotection. We found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca(2+)] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36 +/- 2 (SE)% to 15 +/- 1% with IPC. Bracketing ischemic pulses with 200 microM 5-hydroxydecanoic acid or 10 microM glibenclamide increased infarct size to 28 +/- 3% and 26 +/- 4%, respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia and that this is associated with decreased cytosolic [Ca(2+)] loading and enhanced ATP-sensitive K channel opening.

Adenosine Triphosphate↗
PubMed2002

Anesthetic preconditioning: triggering role of reactive oxygen and nitrogen species in isolated hearts.

We postulated that anesthetic preconditioning (APC) is triggered by reactive oxygen/nitrogen species (ROS/RNS). We used the isolated guinea pig heart perfused with L-tyrosine, which reacts with ROS and RNS to form strong oxidants, principally peroxynitrite (ONOO(-)), and then forms fluorescent dityrosine. ROS scavengers superoxide dismutase, catalase, and glutathione (SCG) and NO. synthesis inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) were given 5 min before and after sevoflurane preconditioning stimuli. Drugs were washed out before 30 min of ischemia and 120 min of reperfusion. Groups were control (nontreated ischemia control), APC (two, 2-min periods of perfusion with 0.32 +/- 0.02 mM of sevoflurane; separated by a 6-min period of perfusion without sevoflurane), SCG, APC + SCG, L-NAME, and APC + L-NAME. Effluent dityrosine at 1 min reperfusion was 56 +/- 6 (SE), 15 +/- 5, 40 +/- 5(++), 39 +/- 4(++), 35 +/- 4(++) , and 33 +/- 5(++) units ((++)P< 0.05 vs. APC), respectively; left ventricular pressure (%baseline) at 60 min of reperfusion was 30 +/- 5(++), 60 +/- 4, 35 +/- 5(++), 37 +/- 5(++), 44 +/- 4, and 47 +/- 4; and infarct size (%total heart weight) was 50 +/- 5(++), 19 +/- 2, 48 +/- 3(++), 46 +/- 4(++), 42 +/- 4(++), and 45 +/- 2(++). Thus APC is initiated by ROS as shown by improved function, reduced infarct size, and reduced dityrosine on reperfusion; protective and ROS/RNS-reducing effect of APC were attenuated when bracketed by ROS scavengers or NO* inhibition.

Anesthetics↗
PubMed2002

Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts.

NADH increases during ischemia because O(2) shortage limits NADH oxidation at the electron transport chain. Ischemic (IPC) and anesthetic preconditioning (APC) attenuate cardiac reperfusion injury. We examined whether IPC and APC similarly alter NADH, i.e., mitochondrial metabolism. NADH fluorescence was measured at the left ventricular wall of 40 Langendorff-prepared guinea pig hearts. IPC was achieved by two 5-min periods of ischemia and APC by exposure to 0.5 or 1.3 mM sevoflurane for 15 min, each ending 30 min before 30 min of global ischemia. During ischemia, NADH initially increased in nonpreconditioned control hearts and then gradually declined below baseline levels. This increase in NADH was lower after APC but not after IPC. The subsequent decline was slower after IPC and APC. On reperfusion, NADH was less decreased after IPC or APC, mechanical and metabolic functions were improved, and infarct size was lower compared with controls. Our results indicate that IPC and APC cause distinctive changes in mitochondrial metabolism during ischemia and thus lead to improved function and tissue viability on reperfusion.

Anesthetics↗
PubMed2002

Improvement of tumor response by manipulation of tumor oxygenation during photodynamic therapy.

Photodynamic therapy (PDT) requires molecular oxygen during light irradiation to generate reactive oxygen species. Tumor hypoxia, either preexisting or induced by PDT, can severely hamper the effectiveness of PDT. Lowering the light irradiation dose rate or fractionating a light dose may improve cell kill of PDT-induced hypoxic cells but will have no effect on preexisting hypoxic cells. In this study hyperoxygenation technique was used during PDT to overcome hypoxia. C3H mice with transplanted mammary carcinoma tumors were injected with 12.5 mg/kg Photofrin and irradiated with 630 nm laser light 24 h later. Tumor oxygenation was manipulated by subjecting the animals to 3 atp (atmospheric pressure) hyperbaric oxygen or normobaric oxygen during PDT light irradiation. The results show a significant improvement in tumor response when PDT was delivered during hyperoxygenation. With hyperoxygenation up to 80% of treated tumors showed no regrowth after 60 days. In comparison, when animals breathed room air, only 20% of treated tumors did not regrow. To explore the effect of hyperoxygenation on tumor oxygenation, tumor partial oxygen pressure was measured with microelectrodes positioned in preexisting hypoxic regions before and during the PDT. The results show that hyperoxygenation may oxygenate preexisting hypoxic cells and compensate for oxygen depletion induced by PDT light irradiation. In conclusion, hyperoxygenation may provide effective ways to improve PDT efficiency by oxygenating both preexisting and treatment-induced cell hypoxia.

Animals↗
PubMed2002

Preclinical studies in normal canine prostate of a novel palladium-bacteriopheophorbide (WST09) photosensitizer for photodynamic therapy of prostate cancers.

Photodynamic therapy (PDT) uses light to activate a photosensitizer to achieve localized tumor control. In this study, PDT mediated by a second-generation photosensitizer, palladium-bacteriopheophorbide WST09 (Tookad) was investigated as an alternative therapy for prostate cancer. Normal canine prostate was used as the animal model. PDT was performed by irradiating the surgically exposed prostate superficially or interstitially at 763 nm to different total fluences (100 or 200 J/cm2; 50, 100 or 200 J/cm) at 5 or 15 min after intravenous administration of the drug (2 mg/kg). Areas on the bladder and colon were also irradiated. The local light fluence rate and temperature were monitored by interstitial probes in the prostate. All animals recovered well, without urethral complications. During the 1 week to 3 month post-treatment period, the prostates were harvested for histopathological examination. The PDT-induced lesions showed uniform hemorrhagic necrosis and atrophy, were well delineated from the adjacent normal tissue and increased linearly in diameter with the logarithm of the delivered light fluence. A maximum PDT-induced lesion size of over 3 cm diameter could be achieved with a single interstitial treatment. There was no damage to the bladder or rectum caused by scattered light from the prostate. The bladder and rectum were also directly irradiated with PDT. At 80 J/cm2, a full-depth necrosis was observed but resulted in no perforation. At 40 J/cm2, PDT produced minimal damage to the bladder or rectum. On the basis of optical dosimetry, we have estimated that 20 J/cm2 is the fluence required to produce prostatic necrosis. Thus, the normal structure adjacent to the prostate can be safely preserved with careful dosimetry. At therapeutic PDT levels, there was no structural or functional urethral damage even when the urethra was within the treated region. Hence, Tookad-PDT appears to be a promising candidate for prostate ablation in patients with recurrent, or possibly even primary, prostate cancer.

Animals↗
PubMed2002

Apoptosis of hepatoma cells SMMC-7721 induced by Ginkgo biloba seed polysaccharide.

AIM: To study the apoptosis of hepatoma cells SMMC-7721 induced by polysaccharide isolated from Ginkgo biloba seed. METHODS: Ginkgo biloba seed polysaccharide (GBSP) was isolated by ethanol fractionation of Ginkgo biloba seed and purified by Sephadex G-200 chromatography. The purity of GBSP was verified by reaction with iodine-potassium iodide and ninhydrin and confirmed by UV spectrophotometer, cellulose acetate membrane electrophoresis and Sepharose 4B gel filtration chromatography. The Scanning Electron Microscope (SEM) and Flow Cytometry (FCM) were used to examine the SMMC-7721 cells with and without GBSP treatment at 500 mg/ml for 36 h. RESULTS: GBSP product obtained was of high purity with the average molecular weight of 1.86 X 10(5). Quantitative analysis of SMMC-7721 cells in vitro with FCM showed that the percentages of G(2)-M cells without and with GBSP treatment were 17.01+/-1.28 % and 11.77+/-1.50% (P<0.05), the debris ratio of the cells were 0.46+/-0.12 % and 0.06+/-0.06 % (P<0.01), and the apoptosis ratio of cells was 3.84+/-0.55 % and 9.13+/-1.48 % (P<0.01) respectively. Following GBSP treatment, microvilli of SMMC-7721 cells appeared thinner and the number of spherical cells increased markedly. Most significantly, the apoptosis bodies were formed on and around the spherical cells treated with GBSP. CONCLUSION: GBSP could potentially induce the apoptosis of SMMC-7721 cells.

Apoptosis↗