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PubMed2006

Transcriptional regulation of catabolic pathways for aromatic compounds in Corynebacterium glutamicum.

Corynebacterium glutamicum is a gram-positive soil microorganism able to utilize a large variety of aromatic compounds as the sole carbon source. The corresponding catabolic routes are associated with multiple ring-fission dioxygenases and among other channeling reactions, include the gentisate pathway, the protocatechuate and catechol branches of the beta-ketoadipate pathway and two potential hydroxyquinol pathways. Genes encoding the enzymatic machinery for the bioconversion of aromatic compounds are organized in several clusters in the C. glutamicum genome. Expression of the gene clusters is under specific transcriptional control, apparently including eight DNA-binding proteins belonging to the AraC, IclR, LuxR, PadR, and TetR families of transcriptional regulators. Expression of the gentisate pathway involved in the utilization of 3-hydroxybenzoate and gentisate is positively regulated by an IclR-type activator. The metabolic channeling of ferulate, vanillin and vanillate into the protocatechuate branch of the beta-ketoadipate pathway is controlled by a PadR-like repressor. Regulatory proteins of the IclR and LuxR families participate in transcriptional regulation of the branches of the beta-ketoadipate pathway that are involved in the utilization of benzoate, 4-hydroxybenzoate and protocatechuate. The channeling of phenol into this pathway may be under positive transcriptional control by an AraC-type activator. One of the potential hydroxyquinol pathways of C. glutamicum is apparently repressed by a TetR-type regulator. This global analysis revealed that transcriptional regulation of aromatic compound utilization is mainly controlled by single regulatory proteins sensing the presence of aromatic compounds, thus representing single input motifs within the transcriptional regulatory network of C. glutamicum.

Biodegradation, Environmental↗
PubMed2006

Radiofrequency current catheter ablation of accessory atrioventricular pathways.

BACKGROUND: The purpose of this study was to evaluate the safety and efficacy of a radiofrequency catheter ablation in the patients with the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardia involving a concealed accessory atrio ventricular connection. METHODS AND RESULTS: During a 45 month period (1st January 2002 until 30th September 2005) 373 consecutive patients underwent electrophysiological study in our electrophysiological lab at the Institute for Heart Diseases. Of all the patients 171 (45.8%) were ablated for junction depend tachycardia. Ninety-five patients had undergone ablation of atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentry tachycardia (AVRT) with accessory pathway (AP) 76 patients. Ablation of the atrioventricular node (AVN) was performed in 59 patients, because of uncontrolled atrial fibrillation with implantation of pacemakers. Ablation was successful in 206 patients (89.3%), partial successful was achieved in 21 patient (9.4%), and no successful only in 3 patients (1.3%). Ablation successful outcome rate was 98.7% (without clinical supraventricular arrhythmia in the follow up period until September 2005). There was a need for performing a re-do ablation in 11 patients (4.8%). A complication occurred in 8 patients, 4.9% (only one major complication, complete atrioventricular block with narrow QRS complex in the AVNRT group). In the group with accessory pathways (atrio ventricular reentry tachycardia (AVRT), there were 76 patients, 28 without delta way on the electrocardiogram (concealed accessory pathways), 47 patients were with open form of accessory pathways, with delta way on EKG (Wolff-Parkinson-White syndrome) and only in one patient with accessory pathway between right atrio and right bundle branch (Mahaim form of concealed accessory pathway). In two patients with AVRT, another circle movement tachycardia was found after the ablation of the accessory pathways, bystander arrhythmia of AVNRT: CONCLUSIONS: The success and safety of catheter accessory pathway ablation is so great that we recommend this nonpharmacological approach as an initial option to any patient with AVRT who has recurrent symptomatic arrhythmias.

Adolescent↗
PubMed1991

Metabolic pathways of apolipoprotein B in heterozygous familial hypercholesterolemia: studies with a [3H]leucine tracer.

The kinetics of apolipoprotein B (apoB) were measured in seven studies in heterozygous, familial hypercholesterolemic subjects (FH) and in five studies in normal subjects, using in vivo tracer kinetic methodology with a [3H]leucine tracer. Very low density (VLDL) and low density lipoproteins (LDL) were isolated ultracentrifugally and LDL was fractionated into high and low molecular weight subspecies. ApoB was isolated, its specific radioactivity was measured, and the kinetic data were analyzed by compartmental modeling using the SAAM computer program. The pathways of apoB metabolism differ in FH and normal subjects in two major respects. Normals secrete greater than 90% of apoB as VLDL, while one-third of apoB is secreted as intermediate density lipoprotein IDL/LDL in FH. Normals lose 40-50% of apoB from plasma as VLDL/IDL, while FH subjects lose none, metabolizing all of apoB to LDL. In FH, there is also the known prolongation of LDL residence time. The leucine tracer, biosynthetically incorporated into plasma apoB, permits distinguishing the separate pathways by which the metabolism of apoB is channeled. ApoB synthesis and secretion require 1.3 h. ApoB is secreted by three routes: 1) as large VLDL where it is metabolized by a delipidation chain; 2) as a rapidly metabolized VLDL fraction converted to LDL; and 3) as IDL or LDL. ApoB is metabolized along two pathways. The delipidation chain processes large VLDL to small VLDL, IDL, and LDL. The IDL pathway channels nascent, rapidly metabolized VLDL and IDL particles into LDL. It thus provides a fast pathway for the entrance of apoB tracer into LDL, while the delipidation pathway is a slower route for channeling apoB through VLDL into LDL. LDL apoB is derived in almost equal amounts from both pathways, which feed predominantly into large LDL. Small LDL is a product of large LDL, and the major loss of LDL-apoB is from small LDL. Two features of apoB metabolism in FH, the major secretory pathway through IDL and the absence of a catabolic loss of apoB from VLDL/IDL, greatly facilitate measuring the metabolic channeling of apoB into LDL.

Adult↗
PubMed1991

Cellular models of macrophage tumoricidal effector mechanisms in vitro. Characterization of cytolytic responses to tumor necrosis factor and nitric oxide pathways in vitro.

The recently described L-arginine-dependent nitric oxide (NO) pathway has been proposed to interact synergistically with the TNF pathway in murine macrophage-mediated tumor cytotoxicity in vitro. We have employed an experimental construct in which these two pathways were independently expressed by two different effector cell populations. The TNF-dependent pathway was committed by murine 3T3 cells transfected with the cDNA encoding human pro-TNF. The NO pathway was executed by the murine EMT-6 mammary adenocarcinoma cell line treated with murine rIFN-gamma and LPS. Controls for the TNF pathway committed by the transfectant included lysis of the TNF-sensitive murine L929 cell in coculture, secretion of TNF, and absence of nitrite synthesis. For the NO pathway controls included lysis of the murine P815 mastocytoma cocultured with activated EMT-6 cells that had been pretreated with murine rIFN-gamma and LPS, production of nitrite by this activated effector cell, and an absence of TNF secretion. The target cell panel included L929, EMT-6, P815, and murine B16 melanoma and TU-5 sarcoma cell lines. All targets on this panel were susceptible to lysis by LPS-triggered murine bacillus Calmette-Guérin-activated macrophages. The 3T3 transfectant caused significant lysis of cocultured L929 and TU-5 targets. The EMT-6 effector cell only caused significant lysis of the P815 target. When both effector cells were cocultured with these target cells, lysis of the P815 target was observed to be additive or superadditive; however, for all the other targets, cytotoxicity was comparable with or subadditive compared with that seen with the 3T3 transfectant effector cell alone. Thus, these two pathways do not appear to account for the broad, potent tumoricidal activity observed for activated macrophages in vitro.

Animals↗
PubMed1989

An alternative pathway of induction of lymphokine production by T lymphocyte clones.

We have previously described a variant murine CTL clone that in contrast to all other clones tested, exhibited a novel capacity to produce IFN-gamma in response to IL-2. This alternative pathway of IFN-gamma induction differed from the conventional TCR complex-mediated pathway in that it was independent of elevated intracellular Ca2+ and insensitive to cyclosporine A. We report here the presence of an analogous pathway in the majority of T lymphocyte clones tested, when these clones are stimulated with IL-2 in the presence of syngeneic or third-party splenocytes. The accessory function of splenocytes in this alternative pathway is mediated by the MAC-1+ subpopulation and apparently involves cell-cell contact. However, the structure with which the MAC-1 antibody reacts probably is not involved directly. No involvement of Ag or the TCR for Ag could be demonstrated in this alternative pathway of lymphokine induction. The array of lymphokines induced by this alternative pathway is only a subset of those induced by antigenic stimulation. Finally, as with the previously described variant clone, IL-2-mediated induction of IFN-gamma production by the normal T lymphocyte clones is independent of normal extracellular Ca2+ levels and insensitive to cyclosporine A. Thus, this alternative pathway of lymphokine induction apparently constitutes a distinct signaling pathway in cloned T lymphocytes.

Animals↗
PubMed1988

[Electrophysiologic properties of accessory atrioventricular pathways. Comparison with myocardial tissue and relation to site].

In 45 patients (15 female, 30 male; age 34 +/- 12 years) with Wolff-Parkinson-White syndrome: 1) the relation between electrophysiologic properties and location of accessory pathways and 2) the relationship between electrophysiologic properties of accessory pathways and adjacent atrial and ventricular myocardium was studied. Location of the accessory pathways was determined by catheter mapping of the coronary sinus and the tricuspid valve ring. There was no linear correlation between antegrade and retrograde effective refractory periods of accessory pathways and adjacent myocardial tissue. According to their location, accessory pathways were divided into right lateral (n = 4), anteroseptal (n = 6), posteroseptal (n = 10), left posterolateral (n = 8), and left lateral (n = 17). While analysis of variance revealed no differences between subgroups concerning retrograde effective refractory periods, antegrade effective refractory periods were significantly different (p less than .01). Moving in a clockwise direction around the mitral valve ring, antegrade effective refractory periods of the accessory pathways decrease from anteroseptal (321 +/- 30 ms) to posteroseptal (290 +/- 38 ms), left posterolateral (258 +/- 21 ms) and left lateral (246 +/- 27 ms), (Spearman R = 0.70m, p less than .01). Antegrade effective refractory periods of septally located accessory pathways (301 +/- 38) were significantly longer than of pathways located in the free wall of the ventricles (251 +/- 24, p less than .01).

Adult↗
PubMed1987

The lymphocyte function-associated antigen (LFA)-1 and CD2/LFA-3 pathways of antigen-independent human T cell adhesion.

Human cytotoxic T lymphocyte clones form conjugates with both antigen-positive and antigen-negative lymphoblastoid cells. Conjugates with antigen-negative targets form as rapidly, and are almost as frequent, as those with antigen-positive targets; both types are strong. Monoclonal antibodies against lymphocyte function-associated antigen (LFA)-1, CD2, and LFA-3 (or their Fab fragments) each consistently inhibit conjugate formation, but only partially; mixes of alpha LFA-1 with either CD2 monoclonal antibodies or alpha LFA-3 cause complete inhibition. Our previous studies have demonstrated two distinct pathways of antigen-independent conjugate (AIC) formation, one involving LFA-1 and the other involving CD2/LFA-3. The present studies showing supra-additive inhibition with mixes of Fab indicate that at least a major fraction of the conjugates involve T cells which utilize both pathways. Preincubation studies (and restricted expression for CD2) demonstrate that in the CD2/LFA-3 pathway, CD2 is critical on the effector and LFA-3 on the target and that in the LFA-1 pathway, LFA-1 is critical on the effector. Analysis of conjugate formation by primary allosensitized T cells confirms the critical findings made with T cell clones. Among a panel of antigen-negative "target" cell lines tested, there is wide variation in the number of AIC formed with cytotoxic T lymphocyte clones; this variation correlates partially with differences in level of expression of LFA-3. Both pathways of adhesion are utilized in AIC formation with all five targets tested, but there was variation between targets in the relative contribution by each pathway. Studies of inhibition of lysis (rather than conjugate formation) support the relevance of the two-pathway model to the lytic process as a whole. These studies demonstrate the general involvement of two pathways of adhesion in human T cell interactions: one involving T cell LFA-1 and the other involving T cell CD2 binding to target cell LFA-3.

Antibodies, Monoclonal↗
PubMed1978

Multiple pathways of DNA repair and their possible roles in mutagenesis.

In studies on bacteria, the excision repair of UVR-induced DNA base damage has been divided into two major pathways on the basis of physiologic requirements and genetic control. The major pathway requires a functional polA+ gene, does not need complete growth medium, is largely error free, and produces short patches during repair. The second pathway requires complete growth medium and functional recA+, recB+, recC+, lexA+, uvrD+, and polC+ genes, is mutagenic, and produces long patches during repair. A second type of ecision repair exists, in which the modified base is removed by a DNA glycosylase, and the chain is nicked by an apurinic (apyrimidinic) acid endonuclease. Subsequent events are presumed similar to the above excision repair process. The postreplication repair system has been divided into at least four distinct pathways, three of which depend on functional recB+, lexA+, and uvrD+ genes, and are error free. A fourth pathway depends on the above gene products but is blocked by postirradiation treatment with chloramphenicol, and may be the UV-inducible, error-prone, mutagenic pathway of repair ("SOS repair"). A possible fifth pathway is dependent on a functional recF+ gene and is independent of the recB+-dependent pathway. Mutagenesis is the result of error-prone DNA repair, and evidence is growing that carcinogenesis is also the result of error-prone repair. Therefore, a complete understanding of DNA repair is crucial to a complete understanding of the molecular basis of carcinogenesis.

DNA Ligases↗
PubMed1985

Dual pathways for the intracellular processing of insulin. Relationship between retroendocytosis of intact hormone and the recycling of insulin receptors.

Adipocytes process insulin through either of two pathways: a retroendocytotic pathway that culminates in the release of intact insulin, and a degradative pathway that terminates in the intracellular catabolism and release of degraded ligand. Mechanistically, these pathways were found to differ in several ways. First, temporal differences were found in the rate at which intact and degraded products were extruded. After 125I-insulin was preloaded into the cell interior, intact ligand was completely released during the first 10 min (t 1/2 = 2 min), whereas degraded insulin was released at a much slower rate over 1 h (t 1/2 greater than 8 min). Secondly, it was found that chloroquine profoundly inhibited the insulin degradative pathway, resulting in the intracellular accumulation of intact ligand and a reduction in the release of degraded products. In contrast, however, chloroquine was without effect on the retroendocytotic processing of insulin. Based on the known actions of chloroquine, it appears that retroendocytosis of insulin does not involve vesicular acidification or dissociation of the insulin-receptor complex and that insulin is most likely carried to the cell exterior in the same vesicles (either receptor-bound or free) as those mediating recycling receptors. Interestingly, accumulation of undergraded insulin within chloroquine-treated cells did not result in the release of additional intact ligand, suggesting that once insulin enters the degradative compartment it is committed to catabolism and cannot exit the cell through the retroendocytotic pathway. A third difference was revealed by the finding that extracellular unlabeled insulin (100 ng/ml) markedly accelerated the rate at which preloaded 125I-insulin was released from adipocytes (t 1/2 of 3 min versus 7 min in controls cells). Analysis of the composition of the released products revealed that extracellular insulin rapidly augmented (over 10 min) in a dose-dependent manner (5-200 ng/ml) the amount of insulin released intact (from 25 to 38% of preloaded counts; insulin ED50 = 10 ng/ml). Although extracellular insulin had no effect on the early extrusion of degraded insulin, the release of catabolized products was reduced at later times. The interpretation of these results is that the rate or amount of incoming insulin-receptor complexes can effect a sorting process (prior to bifurcation) such that a proportion of insulin is shunted from the slower degradative pathway to the more rapid retroendocytotic pathway.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗
PubMed1983

Changes in responsiveness of the beta-adrenergic and serotonergic pathways of the rabbit corneal epithelium.

Adrenergic agonists stimulate the synthesis of cyclic AMP by incubated rabbit corneas with the following order of potency: isoproterenol greater than epinephrine greater than norepinephrine. These agonists have the same order of potency when displacing the specific, beta-adrenergic radioligand, 3H-dihydroalprenolol, from beta-adrenergic receptors on membranes prepared from corneal epithelium. At another locus, serotonin stimulates cyclic AMP synthesis. Inhibition of stimulation in vitro by lysergic acid diethylamide, methysergide, cyproheptadine, and spiroperidol demonstrates the specificity of this pathway for serotonin. Topical epinephrine causes subsensitivity or decreased responsiveness of the beta-adrenergic pathway. There is loss of approximately half the beta-adrenergic receptors from the cornea and a similar loss of epinephrine-stimulated cyclic AMP synthesis, both of which return to control levels in 96 hrs. There is no change in affinity for catecholamines and no loss of responsiveness to prostaglandin E2 or serotonin. Pretreatment with nialamide or subsequent treatment with additional epinephrine does not cause further loss of responsiveness. Supersensitivity or increased responsiveness of this pathway occurs following superior cervical ganglionectomy. Topical serotonin causes decreased responsiveness of the serotonergic pathway. When potentiated by nialamide, serotonin causes almost complete loss of serotonin-stimulated cyclic AMP synthesis for 24-48 hrs. There is no loss of responsiveness to epinephrine. Increased responsiveness of this pathway does not occur following superior cervical ganglionectomy. The authors conclude that the corneal epithelium has both beta 2-adrenergic and serotonin-2 pathways, and each pathway exhibits altered responsiveness by similar mechanisms. In response to exogenous or endogenous stimulation, the beta-adrenergic responsive cells and the serotonergic responsive cells apparently regulate the total number of pathway-specific receptors on their surfaces. Furthermore, the authors postulate that two populations of beta-adrenergic responsive cells exist; those on the apical surface of the epithelium that respond to catecholamine in the tears and those near the basal surface that respond to neuronal catecholamine.

Adrenergic beta-Agonists↗
PubMed1981

Surgical treatment of left free wall accessory pathways of atrioventricular conduction of the Kent type.

This report relates the surgical experience with 79 patients with arrhythmias who had 82 left free wall accessory pathways of atrioventricular conduction of the Kent type. The current operation for the interruption of the pathway consists of two steps. First, the localization of the pathway is done by mapping the epicardial excitation sequence of the atria and the ventricles. This is followed by a set group of maneuvers needed to divide the pathway, which is not visible or palpable. First, an endocardial atrial incision is made just above the anulus fibrosus extending 1.5 to 2.0 cm on each side of the pathway's crossing point. Then, a wide separation of the coronary sulcus fat from the atria and ventricles is done. Finally, superficial fibers of the ventricular myocardium are separated from the anulus fibrosus. The surgical problems such as the possible coronary sinus origin of a pathway and the proximity of pathways to the left fibrous trigone are discussed, both from the electrophysiological and the surgical standpoints. The overall success rate for interruption of left free wall pathways has been 90% with no failure in the last 34 patients.

Adolescent↗
PubMed1995

[Location of atrial and ventricular insertions of accessory atrioventricular pathways using surface ECG mapping and its importance in catheter ablation therapy].

BACKGROUND: The modern non-pharmacological therapy of the WPW syndrome by means of catheter ablation is based on the interruption of the accessory pathway(-s) by radiofrequency current energy. Destruction of the morphologic substrate of the arrhythmia alters the activation wave spread in the heart. OBJECTIVES: It was the aim of this report to demonstrate the diagnostic potential of BSM in localizing both overt and concealed accessory pathways. Presented study analyzes the alterations of the cardioelectric field by means of body surface ECG mapping in two female patients with accessory pathways before and after their successful curative treatment by radiofrequency catheter ablation. METHODS: Five patients were analyzed prior and after RF catheter ablation by BSM, two of them were selected for this presentation. One patient with WPW syndrome suffered from frequent supraventricular tachycardia due to in one female patient with an overt accessory pathway. The other patient was for several years incessantly in permanent junctional reentry tachycardia due to a concealed accessory pathway. The examination comprised 12-lead ECG, orthogonal vectorcardiogram according to Frank, BSM using a regular 80-electrode-array system and signal-averaged ECG. RESULTS: The RF ablation was successful in both patients and their arrhythmia was abolished. By means of a detailed analysis of the ventricular activation prior RF ablation in the patient with WPW syndrome the precise site of the ventricular insertion of the accessory pathway in the left lateral free wall was predicted. Furthermore, alterations of the terminal QRS complex were observed when comparing pre- versus post-ablation maps. In the second patient the atrial insertion of the accessory pathway with retrograde and decremental conduction was successfully localized to the right septal region by means of pre-ablation BSM. CONCLUSIONS: Both ventricular and atrial activation can be in detail analyzed by means of BSM. Such analysis offers more precise information on the spatial component of the activation wave spread. This case report gives further evidence that BSM is a useful method for precise localization of both ventricular and atrial insertion sites of accessory pathways in patients with paroxysmal tachycardias due to this electrophysiologic abnormality. This information gained recently clinical impact since it can be directly used for faster arrhythmogenic substrate targeting during ablation therapy. (Fig. 5, Ref. 17.)

Adolescent↗
PubMed1994

Representations of metabolic knowledge: pathways.

The automatic generation of drawings of metabolic pathways is a challenging problem that depends intimately on exactly what information has been recorded for each pathway, and on how that information is encoded. The chief contributions of the paper are a minimized representation for biochemical pathways called the predecessor list, and inference procedures for converting the predecessor list into a pathway-graph representation that can serve as input to a pathway-drawing algorithm. The predecessor list has several advantages over the pathway graph, including its compactness and its lack of redundancy. The conversion between the two representations can be formulated as both a constraint-satisfaction problem and a logical inference problem, whose goal is to assign directions to reactions, and to determine which are the main chemical compounds in the reaction. We describe a set of production rules that solves this inference problem. We also present heuristics for inferring whether the exterior compounds that are substrates of reactions at the periphery of a pathway are side or main compounds. These techniques were evaluated on 18 metabolic pathways from the EcoCyc knowledge base.

Animals↗
PubMed1995

Classical complement pathway activation on nucleated cells. Role of factor H in the control of deposited C3b.

The restriction of alternative complement pathway activation in fluid phase or on nonactivator surfaces has been described as the major physiologic function of the complement regulatory protein factor H. In this study, we provide evidence that factor H is also a restriction factor of classical pathway activation on the surface of nucleated cells. We found that C3b was rapidly converted to inactivated C3b (iC3b) on human SK-MEL-93-2 melanoma cells after classical pathway activation with the murine monoclonal IgG3 Ab R24 directed against the disialoganglioside surface Ag GD3. The SK-MEL-93-2 cells are nonactivators of the alternative pathway and express neither CR1 (CD35) nor the C3b-cleaving protease p65. The cells are further characterized by the expression of only moderate amounts of DAF (CD55) and approximately 5 x 10(3) MCP (CD46) molecules/cell. FACS analysis and direct quantitation using [125I]factor H revealed high level binding of factor H to the melanoma cells (5.6 x 10(6) molecules/cell) during classical pathway activation. The binding of factor H could be inhibited under conditions that inactivate the classical complement pathway (EGTA and heat treatment), but not by factor B depletion of the serum, demonstrating that classical pathway activation was responsible for factor H binding. Treatment of factor B-depleted serum with neutralizing concentrations of polyclonal anti-factor H resulted in the prolonged presence of intact C3b on the cells and a significantly reduced generation of iC3b. The increased amount of C3b on these cells correlated with a 2.65-fold greater rate of cell death. In contrast, the increase in cell death effected by neutralizing concentrations of anti-CD46 or anti-CD55 Ab was only 0.13- or 0.35-fold, respectively. In addition, the supplementation of serum with purified factor H decreased the extent of lysis of the cells. Collectively, these data provide experimental evidence that factor H, through its cofactor activity for C3b degradation, is involved in the restriction of the classical pathway of complement on the surface of nucleated cells, a function that to date has been exclusively attributed to the membrane regulatory proteins CD35 and CD46.

Complement Activation↗
PubMed1994

Radiofrequency catheter ablation of accessory pathways: the initial experience in Singapore.

Radiofrequency catheter ablation is a recently introduced non-surgical technique for curing patients with arrhythmias as a result of conduction over an accessory pathway in patients with the Wolff-Parkinson-White (WPW) syndrome. We present our initial experience with this technique. There were 90 patients (61 males, 29 females) with a mean age of 37 +/- 14.4 years (range: 13-73 years). All except one were symptomatic with a mean duration of symptoms of 10 +/- 9.4 years (range: 0.1-40 years). The indications for catheter ablation were failure of drug therapy in 71, patient's preference in 10, increased risk of sudden death in 6 and almost incessant tachycardia in 3. The radiofrequency ablation was performed using a deflectable 7 French 4 mm tip electrode catheter positioned at the mitral or tricuspid annulus. The site of the accessory pathway was localised by electrophysiological study and radiofrequency energy applied via the tip of the catheter. There were 100 accessory pathways as 10 (10%) patients had multiple accessory pathways. There were 69 (69%) left free wall, 11 (11%) posteroseptal, 13 (13%) right free wall, 6 (6%) right anteroseptal accessory pathways and one (1%) midseptal accessory pathways. Ninety-six percent (96%) of the accessory pathways were successfully ablated on the first ablation. Two of the 4 initially unsuccessful ablations were successfully reablated, giving an overall success rate of 98%. There were no major complications. In conclusion, radiofrequency catheter ablation of accessory pathways is highly successful and safe and provides a definitive cure for patients with the WPW syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Transcatheter radiofrequency ablation. Early experience with supraventricular tachyarrhythmias related to accessory atrioventricular and dual atrioventricular nodal pathways.

OBJECTIVE: To describe our initial experience with transcatheter radiofrequency ablation, a useful new treatment for supraventricular tachyarrhythmias related to the presence of an accessory atrioventricular (AV) pathway or dual atrioventricular nodal pathways. PATIENTS AND METHODS: One hundred and ten patients, including 77 with accessory pathways, 32 with dual atrioventricular (AV) nodal pathways and one with both, underwent electrophysiological studies and were treated with transcatheter radiofrequency ablation in a large metropolitan teaching hospital. RESULTS: Ninety-five patients (86%) were without evidence of accessory pathway conduction or inducible supraventricular tachycardia and were free of symptoms after a mean follow-up of 13 months (range, 3.0-51 months). Sixty-six of 79 accessory pathways (83.5%) were ablated including 42 of 46 left-sided (91%), 14 of 21 posteroseptal (66%), six of seven anteroseptal (86%), three of four right-sided and one of one midseptal pathways. Thirty-one patients with AV nodal reentry were successfully treated by ablation of either the slow (12 patients) or fast (19 patients) conducting AV nodal pathway. There was a progressive improvement in the success rate of the first procedure from 17% to 64% with the use of large-tip catheters and from 64% to 91% when a purpose-built radiofrequency generator was employed. Complications occurred in nine patients: cardiac tamponade (two patients); mild mitral regurgitation (four); subclavian vein thrombosis (one); transient cerebral ischaemic attack (one); and non-thrombocytic purpuric rash (one). These occurred predominantly during the early experience and were without long-term sequelae. Late in our experience, one patient developed complete atrioventricular block requiring permanent pacemaker implantation. CONCLUSIONS: In this institution, radiofrequency catheter ablation has been a safe and effective treatment strategy for patients with life-threatening or highly symptomatic supraventricular arrhythmias.

Adolescent↗
PubMed1993

Radiofrequency ablation of anomalous cardiac pathways: initial experience.

AIM: To describe the initial experience of radiofrequency ablation of anomalous cardiac pathways in patients with supraventricular tachycardias. METHODS: A total of 10 patients with refractory supraventricular tachycardias mediated by anomalous cardiac pathways underwent electrophysiological assessment and attempted pathway ablation. RESULTS: Seven patients with left free wall atrioventricular pathways (two concealed) and two patients with dual atrioventricular nodal pathways had successful pathway ablations and have had no recurrence of arrhythmia. One patient with a concealed posteroseptal atrioventricular pathway was not able to be ablated. All patients tolerated the initial procedure well, but one developed pericarditis later. CONCLUSION: Radiofrequency ablation promises to be an important new technique for the management of patients with anomalous cardiac pathways and supraventricular tachycardias. Our initial experience has been favourable and comparable to other reported series with a high success rate and infrequent complications.

Adult↗
PubMed1994

Catecholaminergic systems in the zebrafish. II. Projection pathways and pattern of termination of the locus coeruleus.

The locus coeruleus is a widely projecting isthmal noradrenergic nucleus. In the zebrafish, it consists of between three and ten neurons, most of which have multiple, bilaterally projecting axons. Immunohodological studies show that the locus coeruleus provides most, if not all, of the noradrenergic innervation of the brain rostral to the isthmus. The pathways and targets in the zebrafish are similar to ascending coeruleal projections of other vertebrates. Axons ascend through two main pathways: the longitudinal catecholamine bundle and the periventricular catecholamine pathway. The former is a dense meshwork of varicosity-bearing axons which ascends along the lateral longitudinal fasciculus into the mesencephalon. In the posterior tuberal area, this bundle dives ventrally and assumes a lateral position. In the diencephalon, it takes up a position ventral to the medial forebrain bundle, and follows this bundle into the telencephalon, where it joins the medial olfactory tract to enter the olfactory bulb. The periventricular catecholamine pathway is a diffuse pathway consisting of thick, smooth axons. It is associated with the medial longitudinal fasciculus. Rostral to the nucleus of the medial longitudinal fasciculus, this pathway joins the longitudinal catecholamine bundle around the medial forebrain bundle. The periventricular pathway gives rise to coarse terminal arbors with large but sparse varicosities, whereas the longitudinal catecholamine bundle gives rise to terminal plexuses with fine and dense fibers and varicosities. Among the more densely innervated regions are the raphé nucleus, the interpeduncular nucleus, the torus semicircularis, parts of the hypothalamus, and the suprachiasmatic and preoptic areas. The torus longitudinalis, optic tectum, cerebellum, habenular complex, the dorsomedial zone of area dorsalis telencephali, and the olfactory bulb are moderately innervated. The nucleus glomerulosus, the torus lateralis and lateral subnuclei of the nucleus diffusus, and the anterior tuberal nucleus are devoid of noradrenergic innervation.

Animals↗