Electrophysiological characteristic of a patient exhibiting the short-coupled variant of torsade de pointes.

A 41-year-old man was admitted because of syncope. The electrocardiogram showed torsade de pointes (Tdp) with no long QT interval and the coupling interval of the initial beat of Tdp was 240 ms. Heterogeneity of ventricular refractoriness was observed together with shortness of the effective refractory period measured at the right ventricular inflow site where the paced QRS morphology was the same as that of the initial beat of Tdp. Verapamil could suppress frequent ventricular premature complexes with a short coupling interval, which lead to Tdp. Polymorphic ventricular tachycardia was induced by triple ventricular extrastimuli. A pure potassium channel blocker was successful in inhibiting polymorphic ventricular tachycardia inducibility by prolongation of refractoriness. These results suggested that triggered ventricular premature complexes may be represent the initiating mechanism, whereas the shortness of local refractory period and heterogeneity of ventricular refractoriness may play a role in the development and the maintenance of the Tdp.

Molecular cloning and functional characterization of two kinds of betaine-aldehyde dehydrogenase in betaine-accumulating mangrove Avicennia marina (Forsk.) Vierh.

Glycinebetaine is an important osmoprotectant in bacteria, plants, and animals, but only little information is available on the synthesis of glycinebetaine in tree plants. Among four mangrove species, glycinebetaine could be detected only in Avicennia marina. Pinitol was the main osmoprotectant in the other three species. The level of glycinebetaine in A. marina increased under high salinity. Betaine-aldehyde dehydrogenase (BADH) was detected in all four species, but choline monooxygenase could not be detected. A cDNA library was constructed from the leaves of A. marina. Two kinds of BADH cDNAs were isolated, one homologous to the spinach chloroplast BADH, and the other with unique residues SKL at the end of C-terminus. The BADH transcription levels of the former were higher than those of the latter. The levels of the former BADH increased at high salinity whereas those of the latter were independent of salinity. BADHs were expressed in Escherichia coli and purified. Two kinds of A. marina BADHs exhibited similar kinetic and stability properties, but were significantly different from those of spinach BADH. A. marina BADHs efficiently catalyzed the oxidation of betainealdehyde, but not the oxidation of omega-aminoaldehydes and were more stable at high temperature than the spinach BADH.

Acute normovolemic hemodilution for radical prostatectomy: can it replace preoperative autologous blood transfusion?

BACKGROUND: Although preoperative autologous blood donation (PAD) is accepted as a standard of care for radical prostatectomy, it is costly, time-consuming and has risks associated with blood storage. Acute normovolemic hemodilution (ANH) is reported to be less expensive and to preserve blood components more effectively than PAD. In the present study, the efficacy and safety of these two autologous blood-collection techniques were compared. METHODS: The study included 16 consecutive patients scheduled for radical prostatectomy. The first eight patients underwent conventional preoperative autologous blood donation of 400 mL 1 week before the operation (PAD group) and the second eight patients underwent acute normovolemic hemodilution followed by immediate operation (ANH group). All blood collected was transfused in the perioperative period. Preoperative and postoperative hematocrit levels in these two groups were compared. RESULTS: There were no differences in preoperative hematocrit, time of operation or operative blood loss between the two groups. In the ANH group, 1080 +/- 160 mL of blood were collected. The postoperative hematocrit level did not differ significantly between the groups. No patient in either group received allogeneic blood transfusion or experienced an adverse event directly related to blood transfusion. CONCLUSION: The two blood-conservation strategies resulted in similar postoperative hematologic outcomes. Given its advantages, which include lower cost, lower risk and higher convenience, ANH is one of the procedures that may replace conventional PAD for use in radical prostatectomy.

Effects of pinacidil on coronary Ca(2+)-myosin phosphorylation in cold potassium cardioplegia model.

The effects of the potassium (K(+)) channel opener pinacidil (Pin) on the coronary smooth muscle Ca(2+)-myosin light chain (MLC) phosphorylation pathway under hypothermic K(+) cardioplegia were determined by use of an in vitro microvessel model. Rat coronary arterioles (100-260 microm in diameter) were subjected to 60 min of simulated hypothermic (20 degrees C) K(+) cardioplegic solutions (K(+) = 25 mM). We first characterized the time course of changes in intracellular Ca(2+) concentration, MLC phosphorylation, and diameter and observed that the K(+) cardioplegia-related vasoconstriction was associated with an activation of the Ca(2+)-MLC phosphorylation pathway. Supplementation with Pin effectively suppressed the Ca(2+) accumulation and MLC phosphorylation in a dose-dependent manner and subsequently maintained a small decrease in vasomotor tone. The ATP-sensitive K(+) (K(ATP))-channel blocker glibenclamide, but not the nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine methyl ester, significantly inhibited the effect of Pin. K(+) cardioplegia augments the coronary Ca(2+)-MLC pathway and results in vasoconstriction. Pin effectively prevents the activation of this pathway and maintains adequate vasorelaxation during K(+) cardioplegia through a K(ATP)-channel mechanism not coupled with the endothelium-derived NO signaling cascade.

Regulation of coronary myoplasmic Ca(2+)-myosin light chain phosphorylation pathway and vasomotor tone: hyperpolarizing versus depolarizing cardioplegia.

BACKGROUND: This study was designed to compare the effects of hyperpolarizing versus depolarizing cardioplegic solutions on the coronary vasomotor regulation, specifically focusing on coronary myoplasmic Ca2+-myosin light chain (MLC) phosphorylation pathway and beta-adrenergic signal transduction. METHODS: With the use of an in vitro cardioplegic model, rat coronary microvessels loaded with fura-2 were subjected to simulated cold (20 degrees C) cardioplegia and reperfused with Krebs solution for 60 minutes at 37 degrees C. Cardioplegia consisted of either (1) Krebs solution alone (control), (2) Krebs plus adenosine triphosphate-sensitive potassium channel opener (100 micromol/L pinacidil [PCO-CP]), (3) hyperkalemic cardioplegia (K(+) = 25 mmol/L [K-CP]), or (4) K-CP plus magnesium (Mg(2+) = 25 mmol/L; [K/Mg-CP]). RESULTS: At the endpoint of the cardioplegic period, K-CP resulted in a significant increase both in [Ca(2+)](i) and in MLC phosphorylation compared with control (both P <.05). In contrast, PCO-CP did not make any significant difference in these indices compared with control. After reperfusion, the relaxation responses to isoproterenol and forskolin after K-CP were significantly reduced (both P <.05 vs control) but were preserved after PCO-CP. K/Mg-CP provided comparable effects to PCO-CP. CONCLUSIONS: These results suggest that neither an activation of the coronary myoplasmic Ca(2+)-MLC phosphorylation pathway nor beta-adrenergic desensitization seen after exposure to depolarizing cardioplegia occurs with exposure to hyperpolarizing cardioplegia and magnesium-supplemented depolarizing hyperkalemic cardioplegia.

[Recurrent episodes of fever of unknown origin as temporal lobe epilepsy].

A 67-year-old woman was admitted to our department for the recurrent fever of unknown origin that occurred once approximately every 1 month for the last 3 years. No clinical and laboratory abnormality were found, except an interictal EEG showing fronto-temporal spike discharges. During hospitalization a characteristic febrile episode was accompanied by automatism, thereby, it became clear that the undetermined periodic febrile episodes were due to temporal lobe epilepsy. In this case, the thermoregulatory center of the hypothalamus might be symptomatic zone of temporal lobe epilepsy.

Intracellular free calcium accumulation in ferret vascular smooth muscle during crystalloid and blood cardioplegic infusions.

OBJECTIVE: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca2+]i) accumulation and microvascular contractile function were examined. METHODS: Isolated ferret hearts were subjected to hyperkalemic (25 mmol/L K+) blood cardioplegic infusion, hypermagnesemic (25 mmol/L Mg2+, K+-free) crystalloid cardioplegic infusion, or hyperkalemic crystalloid cardioplegic infusion for 1 hour. Coronary arterioles were isolated, cannulated, and loaded with fura 2. Reactivity and [Ca2+]i were assessed with videomicroscopy. [Ca2+]i was measured at baseline and after application of 50 mmol/L KCl. In addition, [Ca2+]i and vascular contraction were measured during exposure to Mg2+ and K+ cardioplegic solution at both 4 degrees C and 37 degrees C. RESULTS: From a baseline [Ca2+]i of 177 +/- 52 nmol/L, K+ cardioplegic infusion (302 +/- 80 nmol/L potassium) markedly increased [Ca2+]i, whereas blood cardioplegic infusion (214 +/- 53 nmol/L) and Mg2+ cardioplegic infusion (180 +/- 42 nmol/L) did not alter [Ca2+]i. Although a difference between groups in percentage contraction after application of 50 mmol/L KCl was not observed, [Ca2+]i increased significantly more in vessels in the control group (764 +/- 327 nmol/L) and the K+ crystalloid cardioplegic infusion group (698 +/- 215 nmol/L) than in vessels in the blood cardioplegic infusion group (402 +/- 45 nmol/L) and the Mg2+ cardioplegic infusion group (389 +/- 80 nmol/L). Mg2+ cardioplegic solution induced no microvascular contraction at either 4 degrees C or 37 degrees C, nor was an increase in [Ca2+]i observed. K+ cardioplegic solution induced microvascular contraction at 37 degrees C but not at 4 degrees C; it increased [Ca2+]i at both 4 degrees C and 37 degrees C. CONCLUSION: An Mg2+-based cardioplegic solution, or appropriate Mg2+ or blood supplementation of a K+ crystalloid cardioplegic solution, may decrease the accumulation of [Ca2+]i in the vascular smooth muscle during ischemic arrest.

Coronary microvascular protection with mg2+: effects on intracellular calcium regulation and vascular function.

The use of Mg2+-supplemented hyperkalemic cardioplegia preserves microvascular function. However, the mechanism of this beneficial action remains to be elucidated. We investigated the effects of Mg2+ supplementation on the regulation of intracellular calcium concentration ([Ca2+]i) and vascular function using an in vitro microvascular model. Ferret coronary arterioles (80-150 micrometer in diameter) were studied in a pressurized (40 mmHg) no-flow, normothermic (37 degrees C) state. Simultaneous monitoring of internal luminal diameter and [Ca2+]i using fura 2 were made with microscopic image analysis. The microvessels (n = 6 each group) were divided into four groups according to the content of MgCl2 (nominally 0, 1.2, 5.0, and 25.0 mM) in a hyperkalemic cardioplegic solution ([K+] 25.0 mM). After baseline measurements, vessels were subjected to 60 min of hypoxia with hyperkalemic cardioplegia (equilibrated with 95% N2-5% CO2) containing each concentration of Mg2+ ([Mg2+]) and were then reoxygenated. During hyperkalemic cardioplegia, [Ca2+]i increased in a time-dependent manner in all groups. In the lower [Mg2+] cardioplegia groups, [Ca2+]i was significantly increased at the end of the 60-min cardioplegic period (247 +/- 44 nM and 236 +/- 49 nM in [Mg2+] 0 and 1.2 mM groups, respectively; both P < 0.05 vs. baseline) with 19.6-17.2% vascular contraction. Conversely, there was no significant [Ca2+]i increase in the higher [Mg2+] cardioplegia groups and less vascular contraction (5.4-4.1%, both P < 0.05 vs. [Mg2+] 1.2 mM group). After reperfusion, agonist (U-46619, thromboxane A2 analog)-induced vascular contraction was significantly enhanced in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was normalized in the higher [Mg2+] cardioplegia groups. Intrinsic myogenic contraction was significantly decreased in the lower [Mg2+] cardioplegia groups (both P < 0.05 vs. control) but was preserved in the higher [Mg2+] cardioplegia groups. These results suggest that supplementation of the solution with >5.0 mM [Mg2+] may prevent hyperkalemic cardioplegia-related intracellular Ca2+ overloading and preserve vascular contractile function in coronary microvessels.

RMA1, an Arabidopsis thaliana gene whose cDNA suppresses the yeast sec15 mutation, encodes a novel protein with a RING finger motif and a membrane anchor.

To identify molecules that function in the plant secretory pathway, we screened for Arabidopsis thaliana cDNA clones that complement the temperature-sensitive (ts), secretion-deficient sec15 mutation of yeast Saccharomyces cerevisiae. RMA1, one of the genes obtained in this screening, suppressed not only the ts growth of sec15 but also its secretory defect. RMA1 is not a structural homologue of SEC15 but encodes a novel 28 kDa protein with a RING finger motif and a C-terminal membrane-anchoring domain. Mutational analysis indicates that the RING finger motif of RMA1 is important for its suppression activity. In Arabidopsis plant, RMA1 is ubiquitously expressed. A search for homologous proteins in the database revealed that Arabidopsis, nematode, mouse and human possess close homologues of RMA1.

Effects of tea infusions of various varieties or different manufacturing types on inhibition of mouse mast cell activation.

We investigated effects of various tea infusions on mast cell activation using mouse mast cells. Among various tea extracts, infusions from cultivar 'Benihomare' and Taiwan lineage strongly inhibited histamine release after Fc epsilon RI cross-linking. Among three types of tea (from cultivar 'Benihomare'), extract from oolong tea or black tea inhibited histamine release more strongly than green tea extract. Furthermore, 'Benihomare' oolong tea extract suppressed tyrosine phosphorylation of cellular proteins after Fc epsilon RI cross-linking, but polyvinyl polypyrrolidone treatment of the extract to remove phenolic compounds, weakened the suppressive effect.

Short report: comparison of the effects of sublingual nifedipine and isosorbide dinitrate on oesophageal emptying in patients with Chagasic achalasia.

The effects of sublingual nifedipine and isosorbide dinitrate on oesophageal emptying were compared in 11 patients with Chagasic achalasia. The oesophageal emptying of a radiolabelled test meal was assessed three times in each patient by a scintigraphic technique. No treatment preceded one of the studies (basal study). Nifedipine (20 mg) by the sublingual route 30 min before the meal, preceded one study. Isosorbide dinitrate, 5 mg by the sublingual route 5 min before the meal, preceded the third study. The order of the studies was allocated randomly for each patient. Oesophageal retention at the completion of the meal was significantly less (P less than 0.01) after isosorbide dinitrate (median: 54%, range: 5-87%) than after sublingual nifedipine (median: 78%, range: 7-99%) or after the control study (median: 83%, range: 5-100%). This difference persisted up to 20 min after the meal. Values measured in the control study and after sublingual nifedipine were not different (P greater than 0.10). These results show that isosorbide dinitrate, but not sublingual nifedipine, enhances oesophageal emptying in Chagasic achalasia.

In vitro formation of mineralized nodules by periodontal ligament cells from the rat.

The purposes of this study were to determine whether periodontal ligament (PDL) cells are capable of producing mineralized nodules in vitro and to analyze ultrastructural features of the nodules. Rat PDL cells were obtained from coagulum in the socket at 2 days after tooth extraction and cultured at confluence in standard medium containing Dulbecco's Modified Eagle's Medium supplemented with 10% FBS and antibiotics. To test mineralized nodule formation, cells were further cultured for an additional 3 weeks in the standard medium containing (1) ascorbic acid (50 micrograms/ml) and sodium beta-glycerophosphate (10 mM), (2) ascorbic acid, sodium beta-glycerophosphate, and dexamethasone (5 microM), or (3) ascorbic acid alone. Cells were then fixed in 2.5% glutaraldehyde, postfixed in 1% OsO4, and prepared for light and electron microscopy. Three-dimensional nodules containing mineralized matrices were formed only when the cells were cultured in the presence of ascorbic acid and dexamethasone. They were composed of multilayered fibroblasts (up to 13 layers), and highly organized collagen fibrils with 64 nm cross-banding patterns between the cell layers. The fibroblasts in the nodules exhibited an elongated shape with a high degree of cytoplasmic polarity throughout the nodule, and have the morphological features of PDL fibroblasts as seen in vivo. Mineral deposition with needle-like crystals was initiated on collagen fibrils located in intercellular spaces of the upper cell layers and became increasingly heavier towards the bottom half of the nodules. X-ray microanalysis and electron diffraction analysis confirmed that mineral deposition contained calcium and phosphate in the form of immature hydroxyapatite.(ABSTRACT TRUNCATED AT 250 WORDS)