No abstract available.
Abdominal Pain* ; Humans

No abstract available.
Abdominal Pain* ; Humans

To evaluate the lipid-lowering effect of lovastatin(Mevacor(R)), lovastatin was administered to 38 patients with non-familial hypertcholesterolemia(>220mg/dl). The analysis of the effect was made with 25 patients(58.2+/-7.5 years ; 13 male, 12 female)who had received lovastatin more than 12 weeks. The drug was administered as a single dose with evening meal 20mg at the begining and adding another 20mg if the total cholesterol level was persistently higher than 200mg/dl at the end of each 4 week-period. 1) Total cholesterol level was decreased from 256.6+/-36.9mg/dl to 20932+/-50.1mg/dl at the end of the 4th week, 201.9+/-44.2mg/dl the 8th week and 203.6+/-39.6mg/dl the 12th week (p<0.001), respectively). 2) Triglyceride level was decreased from 196.4+/-104.1mg/dl to 163.4+/-74.4mg/dl at the end of the 4th week(p<0.05) but no significant change at the end of the 8th week showing 169.8+/-73.2mg/dl and 162.7+/-54.8mg/dl the 12th week(p<0.05). 3) High density lipoprotein cholesterol(HDL-C) level was not significantly changed with the drug during the 12 week treatment period. 4) Low density lipoprotein cholesterol(LDL-C) level was decreased remarkably similar to that of total cholesterol. 5) Total cholesterol/HDL-C ratio was decreased from 5.05+/-0.92 to 4.06+/-1.40 at the end of the 4th week(p<0.05), 3.89+/-0.99 the 8th week(p<0.001). 4.20+/-1.10 the 12th week(p<0.01). 6) LDL-C/HDL-C ratio was decreased from 3.24+/-0.94 to 2.43+/-1.21 at the end of the 4th week(p<0.05), 2.23+/-0.86 the 8th week(p<0.001) and 2.54+/-0.98 the 12th week(p<0.05). 7) There was no significant side effect on lovastatin therapy of 12 weeks duration. 8) The laboratory findings including liver function test, uric acid, creatinine, creatine phosphokinase and blood glucose were not changed significantly. From above results we concluded that lovastatin is safe and effective hypocholesterolemic agent in its clinical use.
Blood Glucose ; Cholesterol ; Creatine Kinase ; Creatinine ; Humans ; Hypercholesterolemia* ; Lipoproteins ; Liver Function Tests ; Lovastatin ; Male ; Meals ; Triglycerides ; Uric Acid

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*

It is well documented that cardiac myxomas are associated with immunologic features that can simulate systemic autoimmune diseases. Recently, it was reported that cardiac myxomas produce IL-6 constitutively, which could partly explain the immunologic features observed in these patients. However, only a few investigators have studied cytokines in regards to symptoms they may cause in patients with cardiac myxoma. Also there is very little information in the literature on the immunohistochmical localization of IL-6. We performed immunobistochemical stains for IL-4, TNF, and IL-6 on paraffm embbeded tissue of cardiac myxoma tissue. A bioassay of IL-6 activity in patient's serum and in cultured cells from fresh myxoma tissue was performed to ascertain the role of these cytokines in myxomas. In this study, we demonstrated inununohistochemically that there was a local overproduction of IL-4, TNF, and IL-6 in cytoplasm of the tumor cells in about half cases. Bioassays of the serum and cultured tumor cells revealed elevated IL-6 activities. Also these findings correlate to production of patient's constitutional symptoms with statistical significance (P<0.05). In conclusion, these results are of considerable importance in understanding the role of IL-4, TNF, and IL-6 in cardiac myxoma patient with constitutional symptoms, and have an impact on strategies for diagnosis and therapy of cardiac myxoma.

The purpose of this study was to evaluate the difference of surface roughness of composite resin according to composite resin type, polishing methods, and use of resin sealant. Two hundred rectangular specimens, sized 8 x 3 x 2 mm, were made of Micro-new (Bisco, Inc., Schaumburg, IL, U.S.A) and Filtek Supreme (3M ESPE Dental Products, St. Paul, MN, U.S.A.), and divided into two groups; Micronew-M group, Filtek Supreme-S group. Specimens for each composite group were subdivided into five groups by finishing and polishing instruments used; M1 & S1 (polyester strip), M2 & S2 (Sof-Lex disc), M3 & S3 (Enhance disc and polishing paste), M4 & S4 (Astropol), and M5 & S5 (finishing bur). Polished groups were added letter B after the application of resin surface sealant (Biscover), eg, M1B and S1B. After specimens were stored with distilled water for 24 hr, average surface roughness (Ra) was taken using a surface roughness tester. Representative specimens of each group were examined by FE-SEM (S-4700: Hitachi High Technologies Co., Tokyo, Japan). The data were analysed using paired t-test, ANOVA and Duncan's tests at the 0.05 probability level. The results of this study were as follows; 1. The lowest Ra was achieved in all groups using polyester strip and the highest Ra was achieved in M5, S5 and M5B groups using finishing bur. On FE-SEM, M1 and S1 groups provided the smoothest surfaces, M5 and S5 groups were presented the roughest surfaces and voids by debonding of filler on the polished specimens. 2. There was no significant difference in Ra between Micronew and Filtek Supreme before the application of resin sealant, but Micronew was smoother than Filek Supreme after the application of resin sealant. 3. There was significant corelation between Ra of type of composite resin and polishing methods before the application of resin sealant (p = 0.000), but no significant interaction between them after the application of resin sealant. On FE-SEM, most of composite resin surfaces were smooth after the application of resin sealant on the polished specimens. 4. Compared with before and after the application of resin sealant in group treated in the same composite and polishing methods, Ra of M4B and M5B was statistically lower than that of M4 and M5, and S5B was lower than that of S5, respectively (p < 0.05). In conclusion, surface roughness by polishing instruments was different according to type of composite resin. Overall, polyester strip produced the smoothest surface, but finishing bur produced the roughest surface. Application of resin sealant provided the smooth surfaces in specimens polished with Enhance, Astropol and finishing bur, but not provided them in specimens polished with Sof-Lex disc.
Polyesters ; Water

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.
Acetylcholine ; Action Potentials ; Adenosine ; Animals ; Atropine ; Carbachol ; Cholinergic Agonists* ; Hand ; Ischemia ; Microelectrodes ; Myocardium* ; Rats*

BACKGROUND: To investigate the role of alpha-adrenergic receptors in the development of delayed afterdepolarization, the effect of alpha-adrenoceptor stimulation and blockade on ouabain induced delayed afterdepolarization(DDAD) was examined in rabbit heart Purkinje fibers. METHODS: Purkinje fibers, taken from adult rabbit(1.8 - 2.0kg) heart anesthetized with penobarbital, were mounted in a Luicite chamber and superfused with Tyrode's solution. The transmembrane potentials were measured by the conventional microelectrode technique while the fibers were being stimulated with rectangular pulses of 50% above threshold voltage. The delayed afterdepolarizations were induced by overdrive excitation in the presence of ouabain. RESULTS: Delayed afterdepolarizations were not observed during superfusion of the control Tyrode's solution containing propranolol(5x10(-7)M). However, the addition of ouabain in the presence of propranolol elicited DADs which were dose-, time- and drive cycle length- dependent. Phenylephrine(PE ; 10(-7)M), and alpha-adrenoceptor agonist, potentiated the ouabain-induced DAD during the initial superfusion(for 10 or 20 min) of the test Tyrode's solution. However, it was followed by attenuating-effects after a superfusion time of 50 to 60 min. Both effects showed ouabain dose-dependence. Ouabain(2x10(-7)M), in the presence of propranolol, depolarized the maximum diastolic potential and shortened the action potential duration, and the addition of PE(10(-7)M) did not affect the characteristics of action potential except a decrease in velocity of phase 0 depolarization. Prazosin, an alpha1-adrenoceptor antagonist, inhibited the PE's enhancing effects of ouabaininduced DDAD at 20 min superfusion, but did not affect the attenuating-effects of PE at 60 min superfusion. On the other hand, yohimbine, an alpha2-adrenoceptor antagonist, did not affect the PE's DAD potentiating-effects at 20 min superfusion, but inhibited the attenunating-effects of PE at 60 min superfusion. CONCLUSION: It is inferred that alpha-adrenergic stimulation induce delayed afterdepolarization and triggered activity in the rabbits, being responsible for the arrhythmia development, and the effects are mainly due to the action of alpha1-subtpe adrenoceptor stimulation.
Action Potentials ; Adult ; Arrhythmias, Cardiac ; Hand ; Heart ; Humans ; Membrane Potentials ; Microelectrodes ; Ouabain ; Prazosin ; Propranolol ; Purkinje Fibers ; Rabbits ; Receptors, Adrenergic, alpha* ; Yohimbine

No abstract available.
Decompression* ; Follow-Up Studies* ; Spine* ; Titanium*

Purpose: Regular aerobic exercise has been recommended as an effective lifestyle strategy for the prevention and treatment of cardiovascular disease. However, it is unclear whether short-term exercise (＜ 6 weeks) can also improve vascular function. Thus, we sought to evaluate the efficacy of short-term spinning exercise to improve vascular function and body composition in young women. Methods: Twelve young women (age, 22±2 years; body mass index, 22.2±3.3 kg/m 2 ) participated in 10 spinning exercise sessions (50 minutes per session including 5 minutes for warm up and cool down) at 60% to 85% age predicted maximal heart rate. Assessments were hemodynamics (heart rate [HR], rate-pressure product [RPP], brachial and central blood pressure) and vascular function (carotid to femoral pulse wave velocity [c-f PWV], augmentation index normalized to a HR of 75 beats [AIx@75], brachial artery flow-mediated dilation [FMD]), and body composition. All measurements were obtained at baseline before (test 1 [T1] and test 2 [T2]) and again after completion of the last spinning exercise session (test 3 [T3]). Results: Short-term spinning exercise reduced c-f PWV (T1 : 6.2±0.7 m/sec, T3 : 5.7±0.6 m/sec, p=0.012), AIx@75 (T1: 2.4%±8.8%, T3: −5.9%±9.3%, p＜ 0.001) and increased brachial artery FMD (T1: 8.0%±4.0%, T3: 11.8%±5.4%, p=0.002). Percent body fat also decreased after short-term spinning exercise (T1 : 29.3%±6.0%, T3 : 28.4%±6.1%, p=0.011). In addition, all participants achieved 100% adherence. Conclusion These findings provide preliminary evidence for the effects of short-term spinning exercise to improve vascular function and body composition in young women.