Comparative cytotoxicity of five root canal sealers on cultured human periodontal ligament fibroblasts.

AIM: To evaluate the cytotoxicity of current root canal sealers to periodontal ligament (PDL) fibroblasts. METHODOLOGY: Five root canal sealers (Canals, Canals-N, Topseal, Sealapex, Tubliseal) were prepared and placed into transwells. After initial setting for 1 h, the transwells with sealers were placed into cultured PDL fibroblasts. They were cultured for further 3 or 18 h. Morphological changes were observed. Cell viability was estimated by 3-(4,5-dimethyl-thiazol-2-yl)-2,5- diphenyl-tetrazolium bromide (MTT) assay. RESULTS: Marked retraction and death of PDL fibroblasts were observed after exposure to Canals or Topseal for 3 h. A 3-h exposure of PDL fibroblasts to Tubliseal stimulated MTT reduction. Canals-N showed little cytotoxicity even after an exposure of 18 h. CONCLUSION: Canals was the most toxic sealer, followed by Topseal. Sealapex and Tubliseal had comparable and moderate cytotoxicity to PDL fibroblasts, whereas Canals-N showed little cytotoxicity. Exposure to Tubliseal may modulate MTT reduction in PDL fibroblasts. Canals-N had good biocompatibility.

Localization, dynamics, and protein interactions reveal distinct roles for ER and Golgi SNAREs.

ER-to-Golgi transport, and perhaps intraGolgi transport involves a set of interacting soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins including syntaxin 5, GOS-28, membrin, rsec22b, and rbet1. By immunoelectron microscopy we find that rsec22b and rbet1 are enriched in COPII-coated vesicles that bud from the ER and presumably fuse with nearby vesicular tubular clusters (VTCs). However, all of the SNAREs were found on both COPII- and COPI-coated membranes, indicating that similar SNARE machinery directs both vesicle pathways. rsec22b and rbet1 do not appear beyond the first Golgi cisterna, whereas syntaxin 5 and membrin penetrate deeply into the Golgi stacks. Temperature shifts reveal that membrin, rsec22b, rbet1, and syntaxin 5 are present together on membranes that rapidly recycle between peripheral and Golgi-centric locations. GOS-28, on the other hand, maintains a fixed localization in the Golgi. By immunoprecipitation analysis, syntaxin 5 exists in at least two major subcomplexes: one containing syntaxin 5 (34-kD isoform) and GOS-28, and another containing syntaxin 5 (41- and 34-kD isoforms), membrin, rsec22b, and rbet1. Both subcomplexes appear to involve direct interactions of each SNARE with syntaxin 5. Our results indicate a central role for complexes among rbet1, rsec22b, membrin, and syntaxin 5 (34 and 41 kD) at two membrane fusion interfaces: the fusion of ER-derived vesicles with VTCs, and the assembly of VTCs to form cis-Golgi elements. The 34-kD syntaxin 5 isoform, membrin, and GOS-28 may function in intraGolgi transport.

Uranium distribution in separated clinopyroxenes from four eclogites.

Uranium concentrations and distributions in separated clinopyroxenes of eclogites from four different sites have been studied by the fission track method. Types of uranium occurrences included (i) inhomogeneously distributed clusters, (ii) line concentrations at cracks, and (iii) uniform distributions in the body of the mineral. Different grains from the same sample generally vary by factors of 2 to 4 in uniformly distributed uranium concentration. Samples from different locations vary in their average uniformly distributed uranium concentration by a factor of approximately 1000 (that is, from 0.01 to 20 parts per billion of uranium). The degree of homogeneity also varies markedly from one site to the next. The clinopyroxenes from the only oceanic locality studied (Salt Lake Crater) contained both the largest concentration of uranium (15 to 20 parts per billion) and the most uniform uranium distribution. This study suggests that, if total uranium concentrations in eclogitic clinopyroxenes are less than a few parts per billion, much if not most of the uranium may occur as contaminants along cracks or in microinclusions of unknown origin.

Pre-excited RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome: influence of the atrioventricular node refractory period.

The ventricular rate and percent of pre-excited QRS complexes during atrial fibrillation were compared in two groups of patients with the Wolff-Parkinson-White syndrome. Group A consisted of 22 patients whose anterograde effective refractory period of the accessory pathway was longer than that of the atrioventricular (AV) node. Group B consisted of 23 patients in whom this relation was reversed. No patient had organic heart disease. Both groups had a similar effective refractory period of the accessory pathway (288 +/- 37 vs. 280 +/- 26 ms), whereas that of the AV node was shorter in group A than group B (242 +/- 25 vs. 285 +/- 27 ms, p = 0.0001). Patients in group A had a lower percent of pre-excited QRS complexes during atrial fibrillation (39 +/- 43% vs. 93 +/- 20%, p = 0.0001). In the 21 patients whose refractory period was measured, the difference was plotted against the percent of pre-excited QRS complexes; there was a significant correlation between the two (r = -0.83, p less than 0.001). In patients in whom pre-excited RR intervals were present, the pre-excited RR intervals were compared between the two groups. Both groups had similar effective refractory periods of the accessory pathway (265 +/- 22 vs. 280 +/- 27 ms) and ventricle (200 +/- 17 vs. 211 +/- 26 ms). The effective refractory period of the AV node was shorter in group A (248 +/- 22 vs. 285 +/- 28 ms, p = 0.0005). The shortest pre-excited RR interval did not show any difference (244 +/- 37 vs. 265 +/- 41 ms). However, both the average (328 +/- 39 vs. 397 +/- 56 ms, p = 0.001) and longest (495 +/- 109 vs. 666 +/- 205 ms, p = 0.02) pre-excited RR intervals were shorter in group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment of ventricular tachycardia using an automatic scanning extrastimulus pacemaker.

A patient with recurrent sustained ventricular tachycardia that was resistant to both conventional and experimental antiarrhythmic agents was treated with a programmable automatic scanning extrastimulus pacemaker. The antitachycardia pacemaker was implanted only after many episodes of spontaneous and laboratory-induced ventricular tachycardia were reliably and reproducibly terminated with programmed ventricular extrastimuli. In the 6 months since implantation of the automatic scanning pacemaker, all episodes of ventricular tachycardia have been terminated successfully by the pacemaker. Acceleration of rate of ventricular tachycardia or induction of ventricular fibrillation did not occur at any time during attempted termination of ventricular tachycardia by the pacemaker. The advantages of the automatic scanning extrastimulus pacemaker over other antitachycardia pacemakers are discussed.

Carbamazepine-induced cardiac dysfunction. Characterization of two distinct clinical syndromes.

A patient with sinus bradycardia and atrioventricular block, induced by carbamazepine, prompted an extensive literature review of all previously reported cases. From the analysis of these cases, two distinct forms of carbamazepine-associated cardiac dysfunction emerged. One patient group developed sinus tachycardias in the setting of a massive carbamazepine overdose. The second group consisted almost exclusively of elderly women who developed potentially life-threatening bradyarrhythmias or atrioventricular conduction delay, associated with either therapeutic or modestly elevated carbamazepine serum levels. Because carbamazepine is widely used in the treatment of many neurologic and psychiatric conditions, the recognition of the latter syndrome has important implications for the use of this drug in elderly patients.

Verapamil plasma levels and ventricular rate response in patients with atrial fibrillation and flutter.

The acute effect of verapamil on the ventricular rate in atrial fibrillation and flutter was studied in 15 patients, 13 of whom had heart rate inadequately controlled with digitalis. Plasma concentrations were measured 5 and 10 min after intravenous doses of 0.075 mg/kg and 0.15 mg/kg verapamil. In 9 patients who were clinically compensated, the 0.075-mg dose alone decreased the ventricular rate to under 100/min (responders); in the remaining 6, who had acute congestive heart failure manifested by orthopnea, rales, and pulmonary congestion, ventricular rates were above 100/min after the 0.075-mg dose (nonresponders). The 6 nonresponders received the 0.15-mg dose 30 min later. In all, the response was greater when plasma drug concentration rose after the high dose, although the rate decrease was smaller than in the 9 compensated patients who received the low dose. These results can be explained by assuming an antagonism of the verapamil effect by sympathetic stimulation in nonresponders.

Effect of lidocaine on escape rate in patients with complete atrioventricular block: B. Proximal His bundle block.

Lidocaine was administered intravenously (a loading dose of 1.5 mg/kg body weight followed by a 3 mg/min infusion) to 10 patients with complete atrioventricular (A-V) block proximal to the His bundle and A-V junctional escape rhythm. A-V block was not due to an acute myocardial infarction in seven patients (group I) and was due to an acute inferior wall infarction in three patients (group II). Lidocaine had either no or only a slight depressant effect on the rate of the escape pacemaker in patients in group I but caused severe bradycardia or asystole in two of three patients in group II. Lidocaine had no consistent effect on the atrial rate and did not change the QRS duration and H-V intervals in any patient. These observations are consistent with the results of animal studies that showed that lidocaine selectively depressed conduction in ischemic or depolarized myocardium. The findings also suggest that the use of lidocaine without prior insertion of a pacemaker is unsafe in patients with acute myocardial infarction and complete A-V block proximal to the His bundle.

Coexistence of ventricular parasystole and ventricular couplets: mechanism and clinical significance.

In 78 consecutive patients with uniform ventricular ectopic complexes and without heart disease, ventricular couplets were present significantly more often when the coupling interval of ventricular ectopic complexes was variable than when it was fixed (P less than 0.04). In 69 consecutive patients with couplets, the prevalence of a variable coupling interval was significantly greater than that of (55 versus 14 cases; P less than 0.001). Among 55 patients with a variable coupling interval, ventricular parasystole was probable in 38 and possible in 17 patients. These results suggest that the association between ventricular couplets and parasystole is not coincidental. Of several possible mechanisms responsible for this association reentry within the parasystolic focus or its vicinity is the most probable. This may explain the observation that the couplets are seldom followed by consecutive ventricular ectopic complexes or ventricular tachycardia. If this hypothesis is correct, the clinical significance of ventricular couplets in the presence of ventricular parasystole may be similar to that of single reentrant ventricular ectopic complexes.

Ventricular monophasic action potential changes associated with neurogenic T wave abnormalities and isoproterenol administration in dogs.

Changes in the duration of monophasic action potentials on the anterior and posterior walls of the dog ventricle were correlated with changes in T wave polarity and duration of the Q-T interval after (1) left stellate ganglion transection, (2) right stellate ganglion stimulation, and (3) administration of isoproterenol before or after these procedures. Left stellate ganglion transection and right stellate ganglion stimulation produced similar changes in T wave polarity, but the former prolonged and the latter shortened the Q-T interval. All procedures changed the duration of the monophasic action potential and the Q-T interval in the same direction. The reversal of T wave polarity induced by left stellate ganglion transection, right stellate ganglion stimulation or administration of isoproterenol after left stellate ganglion transection was associated with an average change of 13 to 17 msec in the difference between the monophasic action potential durations on the anterior and posterior ventricular walls. Isoproterenol restored to normal the neurogenic T wave abnormalities produced by left stellate ganglion transection and right stellate ganglion stimulation. The drug shortened the previously prolonged monophasic action potential more than the normal monophasic action potential, and the normal monophasic action potential more than the previously shortened monophasic action potential. This study confirms that the T wave is a sensitive indicator of relatively small changes (less than 20 msec) in the sequence of ventricular repolarization and explains the mechanism by which isoproterenol "normalizes" the primary T wave abnormalities.

Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

This report examines whether in the Cardiac Arrhythmia Suppression Trial death and cardiac arrest from encainide, flecainide and moricizine during the titration phase and from encainide and flecainide during the follow-up phase were related to presence (Q-wave acute myocardial infarction [Q-AMI]) or absence (non-Q-AMI) of pathologic Q waves. In all, 2,371 patients (70% with Q-AMI, 26% with non-Q-AMI, and 4% unknown) entered the titration phase, starting 117 +/- 163 days after index AMI and lasting for an average of 21 days. For the titration phase, no significant differences existed between Q-AMI and non-Q-AMI patients for death and cardiac arrest rate, ventricular premature complex suppression rate, and nonrandomization rate. A total of 1,498 patients entered the follow-up phase of an average of 10 months (starting 129 +/- 158 days after the index AMI), and were randomized to encainide or flecainide, or their matching placebos. In the placebo group, non-Q-AMI patients had a significantly lower rate of death and cardiac arrest than Q-AMI patients (1.0 and 4.6%, respectively; p = 0.04). Encainide and flecainide significantly elevated death and cardiac arrest rate in both non-Q-AMI patients (8.7%, p less than 0.01) and Q-AMI patients (7.8%, p = 0.04). The relative risk for encainide or flecainide over placebo in the non-Q-AMI patients was 8.7, which was significantly higher than 1.7 observed for the Q-AMI patients (p = 0.03). None of the baseline characteristics had any significant interaction with encainide or flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of verapamil on an accessory pathway manifesting as "fatigue phenomenon" in Wolff-Parkinson-White syndrome.

Electrophysiologic study was performed in a 52-year-old man with type A ventricular preexcitation. An accessory atrioventricular pathway with no ventriculoatrial conduction was localized to the posteroseptal region. "Fatigue phenomenon," defined as suppression of atrioventricular conduction following rapid pacing, was observed to be provoked by atrial pacing in a rate- and duration-dependent manner. Administration of 5 mg of intravenous verapamil during sinus rhythm abolished the delta waves. These observations may indicate that pathologic changes in the accessory pathway are responsible for these phenomena.

Results and patterns of perioperative myocardial infarction.

Myocardial injury during a variety of cardiac surgical operations was determined in 57 patients by serial electrocardiograms (ECG's), serial determinations of serum creatine phosphokinase (CPK), and perioperative and postoperative technetium-99m stannous pyrophosphate (PYP) scans. ECG evidence of injury developed in four patients, whereas positive localized injury by PYP scan developed in ten. Twenty-one patients had elevated CPK enzymes postoperatively. The localization of injury by PYP scan correlated with ECG evidence of infarction in only one of four patients. Localized left ventricular injury by PYP scan without new Q waves on the ECG was common (5/12) in patients undergoing aortic valve replacement with perfusion of the coronary arteries. The injury in patients with congenital heart disease occurred at sites of ventricular incision or suggested possible air embolization of the coronary arteries. Perioperative infarction is frequently segmental and nontransmural and occurs in patients with coronary, valvular, and congenital heart disease.

Relationship between respiratory muscle function and age, sex, and other factors.

To investigate the effects of gender and age on respiratory muscle function, 160 healthy volunteers (80 males, 80 females) were divided into four age groups. Twenty-eight of the male subjects were smokers. After the subjects were familiarized with the experimental procedure, respiratory muscle strength, inspiratory muscle endurance, and spirometric function, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, tidal volume, breathing rate, and duty cycle, were measured. The respiratory muscle strength was indicated by the maximal static inspiratory and expiratory pressures (PImmax and PEmmax). Inspiratory muscle endurance was determined by the time the subject was able to sustain breathing against an inspiratory pressure load on a modified Nickerson-Keens device. The results showed that 1) except for inspiratory muscle endurance and FEV1/FVC, men had greater respiratory muscle and pulmonary functions than women, 2) respiratory muscle function and pulmonary function decreased with age, 3) smoking tended to lower duty cycle and FEV1/FVC and to enhance PE,mmax, and 4) inspiratory muscle endurance was greater in men who were physically active than in those who were sedentary. Therefore we conclude that there are sexual and age differences in respiratory muscle strength and pulmonary function and that smoking or physical activity may affect respiratory muscle function.

Exacerbation of insulin resistance and postprandial triglyceride response in newly diagnosed hypertensive patients with hypertriglyceridaemia.

The purpose of the study is to examine the differences in insulin resistance and postprandial triglyceride (TG) response between hypertensive patients with or without hypertriglyceridaemia. The study is a comparative cohort study with matching. Thirty-one newly diagnosed hypertensive patients without any medication were recruited from a health survey. The participants were further divided into two groups: those with fasting TG <2.26 mmol/L, and those with TG between 2.26 and 5.65 mmol/L. Both groups were matched in age, sex, body mass index and waist circumference. Each patient received a 75-g oral glucose tolerance test, an insulin suppression test, and a 1000 kcal high fat mixed meal test. The hypertriglyceridaemic hypertensive patients had significantly higher fasting insulin, 2-h plasma glucose, 2-h insulin, and steady-state plasma glucose (SSPG) (13.16 +/- 1.87 vs 9.76 +/- 3.18 mmol/L). They also had a greater postprandial TG response to the challenge of mixed meal (DeltaAUC 20.76 +/- 10.06 vs 7.97 +/- 3.18 mmol 8 h/L). The postprandial TG response was closely correlated (r = 0.72-0.95, P < 0.0001) with fasting TG in all hypertensive patients. Both fasting TG levels and postprandial TG response were significantly (P < 0.05) correlated with SSPG. In conclusion, the hypertensive patients with hypertriglyceridaemia were more insulin resistant than those without it. Exacerbation of postprandial hypertriglyceridaemia was identified in these patients. The TG response to the challenge of high fat meal was significantly correlated with fasting TG and insulin resistant in them. The results provide a rationale for the alleviation of insulin resistance and hypertriglyceridaemia in these atherosclerosis-prone hypertensive patients.

Using semi-automated oscillometric blood pressure measurement in diabetic patients and their offspring.

To determine whether a semi-automatic oscillometric blood pressure (BP) monitor Dinamap 1846SX (DIN) can replace the standard mercury sphygmomanometer (SMS) for BP measurements in diabetic patients and their offspring, we compared SMS with DIN in 105 diabetic patients and their families. Their mean age was 50.6 (range 24-86) years, of whom 41 had diabetes mellitus (DM), 32 impaired glucose tolerance and 32 non-DM. After resting quietly for 10 min, their right arm BP were measured twice with each device at random and with 1-min intervals between each measurement. Agreement between measurements was tested by plotting the differences between the methods against means and by intraclass correlation coefficient (r(I)). The DIN was also evaluated by the criteria of American Association for the Advancement of Medical Instrumentation (AAMI), the British Hypertension Society (BHS) criteria and clinical criteria of O'Brien. All measurements by DIN [first readings or averaged readings of duplicate measurements of systolic BP (SBP) or diastolic BP (DBP)] satisfied the AAMI criteria and had good agreement with SMS (r(I)=. 951 for SBP and r(I)=.905 for DBP). The first readings of systolic BP measured by DIN vs. SMS failed to satisfy the criteria by O'Brien and reached BHS grade C level. Other measurements passed the limits of O'Brien and reached BHS grade A or B. In conclusion, averaged readings of duplicate BP measurements by DIN are interchangeable with that by SMS in Chinese diabetic patients and their offspring. Only one single DIN measurement is not acceptable for clinical application.

Insulin sensitivity in Chinese ovo-lactovegetarians compared with omnivores.

AIM: To compare the insulin sensitivity indices between Chinese vegetarians and omnivores. METHODS: The study included 36 healthy volunteers (vegetarian, n=19; omnivore, n=17) who had normal fasting plasma glucose levels. Each participant completed an insulin suppression test. We compared steady-state plasma glucose (SSPG), fasting insulin, the homeostasis model assessment for insulin sensitivity (HOMA-IR and HOMA %S) and beta-cell function (HOMA %beta) between the groups. We also tested the correlation of SSPG with years on a vegetarian diet. RESULTS: The omnivore subjects were younger than the vegetarians (55.7+/-3.7 vs 58.6+/-3.6 year of age, P=0.022). There was no difference between the two groups in sex, blood pressure, renal function tests and lipid profiles. The omnivores had higher serum uric acid levels than vegetarians (5.25+/-0.84 vs 4.54+/-0.75 mg/dl, P=0.011). The results of the indices were different between omnivores and vegetarians (SSPG (mean+/-s.d.) 105.4+/-10.2 vs 80.3+/-11.3 mg/dl, P<0.001; fasting insulin, 4.06+/-0.77 vs 3.02+/-1.19 microU/ml, P=0.004; HOMA-IR, 6.75+/-1.31 vs 4.78+/-2.07, P=0.002; HOMA %S, 159.2+/-31.7 vs 264.3+/-171.7%, P=0.018) except insulin secretion index, HOMA %beta (65.6+/-18.0 vs 58.6+/-14.8%, P=0.208). We found a clear linear relation between years on a vegetarian diet and SSPG (r=-0.541, P=0.017). CONCLUSIONS: The vegetarians were more insulin sensitive than the omnivore counterparts. The degree of insulin sensitivity appeared to be correlated with years on a vegetarian diet.

Application of representational difference analysis to cloning a Mycoplasma arthritidis specific DNA fragment.

Representation difference analysis (RDA) was applied to isolate a Mycoplasma arthritidis specific DNA fragment. The DNA fragment obtained was verified to be M. arthritidis specific by polymerase chain reaction (PCR) and dot blot hybridization tests. The size of this fragment was 194 bp and the nucleotide sequence was also determined.

Antimicrobial resistance and serotype distribution of Streptococcus pneumoniae infections in Kaohsiung from 1996 through 1999.

A total of 89 isolates of Streptococcus pneumoniae were obtained from 86 patients during the period from November 1996 through September 1999 at the Kaohsiung Medical University Hospital. The purpose of this study was to determine the antimicrobial susceptibilities and the distribution of serotypes of these isolates, and to correlate these findings with the clinical characteristics of patients. Twenty-one (23.6%) isolates were obtained from patients aged below 5 years, and 38 (42.7%) from patients aged over 65 years. These 86 patients included 53 pneumonia, 13 bacteremia (including 6 with septic shock), 8 urinary tract infection, 8 soft tissue infections, 7 acute exacerbation of chronic bronchitis, 2 ophthalmic infection, and 2 cholecystitis cases. The most frequent serotypes were types 20 (10.1%), 6 (9%), 10 (9%), 11 (9%), and 23 (9%). All isolates were included in the serotypes represented in the 23-valent pneumococcal vaccine. Thirty-four (38.2%) isolates showed reduced penicillin susceptibility by the E-test. The predominant serotypes of penicillin-resistant S. pneumoniae were types 11 (17.6%), 7 (14.7%), 6 (8.8%), 8 (8.8%), and 23 (8.8%). All isolates were susceptible to vancomycin. Resistance rate to erythromycin was 49.4%, chloramphenicol, 20.2%; and trimethoprim/sulfamethoxazole, 61.8%. Multiple resistance (> or = 3 classes of antibiotics) was found in 28 (31.5%) isolates, of which the majority were serotypes 11 (14.3%), 7 (14.3%), 6 (10.7%), 8 (10.7%), and 23 (10.7%).

Mediodorsal nucleus of the thalamus is critical for the expression of memory of methamphetamine-produced conditioned place preference in rats.

Methamphetamine (MA) is a powerful and highly addictive psychostimulant. However, the neural substrate mediating MA-induced conditioned effects, an essential part of addiction, remain unclear. The present study investigated the involvement of the anterior cingulate cortex (ACC), the lateral nucleus of amygdala (LNA), and the mediodorsal nucleus of the thalamus (MD) in MA-conditioned place preference (CPP). Rats underwent bilateral radio-frequency lesions of the ACC, LNA, or MD followed by MA CPP training. Lesions of the MD, but not the ACC or LNA, disrupted MA CPP learning. To clarify the role of the MD on the different stages of the MA CPP memory process, bilateral microinfusions of lidocaine into the MD were performed 5 min prior to each conditioning trial, immediately after the conditioning trial, or 5 min before the testing phase. Pretesting, but not pre- or post-conditioning, infusions of lidocaine into the MD impaired MA CPP. Furthermore, a clear preference for the previously conditioned MA paired cues was expressed when the rats were tested again 24 h after infusions of lidocaine. These results are interpreted as indicating that the MD is specifically involved in the memory retrieval process of MA associated memory which suggests the MD could have an important role in relapse in individuals suffering from MA addiction.