Properties of a Resiniferatoxin-stimulated,Calcium Inhibited but Phosphatidylserine-dependent Kinase,which is Distinct from Protein Kinase C Isotypes α, β1γ, δ, ε and η

We have separated a resiniferatoxin-stimulated histone-kinase activity from human neutrophils, elicited mouse macrophages and murine alveolar macrophages by hydroxyapatite chromatography. The assay conditions for resiniferatoxin kinase were optimized as part of this study and in the presence of phosphatidylserine but absence of Ca²⁺ the K_a for histone IIIs phosphorylation by resiniferatoxin was calculated as 16 nm . Using a phosphate gradient of 20–500 mm , peaks of protein kinase C activity could be washed from the hydroxyapatite column in 300 nm phosphate and resiniferatoxin kinase recovered in 500 mm phosphate. At the optimum concentration of 160 nm , the ability of resiniferatoxin to induce enzyme activity was compared with a range of phorbol esters all at the same concentration. These related compounds failed to activate resiniferatoxin kinase although they have previously been shown to activate protein kinase C isotypes. Similarly sn-1,2,-dioleoylglycerol and the potent irritant capsaicin at 30 μm failed to activate the kinase. A Scatchard analysis of [³H] phorbol dibutyrate binding produced a linear plot (K_d 41·6 nm ; B_max 11·6 fmol unit^?1) and binding was inhibited by resiniferatoxin and 12-O-tetradecanoylphorbol-13-acetate (TPA), with resiniferatoxin 700 times more potent than TPA in this respect. A radiolabeled resiniferatoxin binding assay was also used to demonstrate specific binding of [³H]resiniferatoxin which could be inhibited by unlabelled compound. Resiniferatoxin kinase activity was shown to be distinct from the protein kinase C isotypes α, β₁, γ δ and ε by means of immunological analysis and from the η isotype, because that isotype was not stimulated by resiniferatoxin but was stimulated by TPA when a pseudosubstrate was used. In addition the resiniferatoxin-stimulated activity was inhibited in-vitro by the addition of Ca²⁺ (K_i 0·1-0·5 nm free Ca²⁺). Further purification of resiniferatoxin kinase by Superose chromatography indicated a major activity fraction of about 70–90 kDa. Thus resiniferatoxin kinase, isolated from human and mouse inflammatory cells is distinct from the known isotypes of protein kinase C and is a major resiniferatoxin receptor.     

NASPE POLICY STATEMENT The NASPE* BPEG** Defibrillator Code

BERNSTEIN, A.D., et al .: The NASPE/BPEG Defibrillator Code. A new generic code, patterned after and compatible with the NASPE/BPEG Generic Pacemaker Code (NBG Code) was adopted by the NASPE Board of Trustees on January 23, 1993. It was developed by the NASPE Mode Code Committee, including members of the North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG). It is abbreviated as the NBD (for NASPE/BPEG Defibrillator) Code. It is intended for describing the capabilities and operation of implanted cardioverter defibrillators (ICDs) in conversation, record keeping, and device labeling, and incorporates four positions designating: (1) shock location; (2) antitachycardia pacing location; (3) means of tachycardia detection; and (4) antibradycardia pacing location. An additional Short Form, intended only for use in conversation, was defined as a concise means of distinguishing devices capable of shock alone, shock plus antibradycardia pacing, and shock plus antitachycardia and antibradycardia pacing. (PACE, Vol. 16, September 1993)     

MID-LATENCY AUDITORY EVOKED POTENTIALS DURING KETAMINE ANAESTHESIA IN HUMANS

We studied mid-latency auditory evoked potentials (MLAEP) duringinduction of general anaesthesia with ketamine 2 mg kg^–1MLAEP were recorded before, during and after induction of generalanaesthesia on the vertex (positive) and mastoid (negative)positions. Latencies of the peak V, Na, Pa, Nb, P1 and amplitudesNa/Pa, Pa/Nb and Nb/P1 were measured. Fast-Fourier transformationwas used to calculate power spectra of the MLAEP. In the awakestate, MLAEP had large peak-to-peak amplitudes and a periodicwaveform. Peak latencies remained within the normal range. Powerspectra indicated high energy in the 30–40 Hz frequencyrange. After induction of general anaesthesia with ketamine,there was no change in latency of peaks V. Na, Pa, Nb, P1 andno apparent reduction in amplitudes Na/Pa, Pa/Nb and Nb/P1.In the power spectra, frequencies in the range of 30–40Hz retained high energy. Amplitudes and latencies of MLAEP didnot change during induction of general anaesthesia with ketamine.Primary processing of auditory stimuli in the primary auditorycortex seemed to be preserved under ketamine. Suppression ofsensory (auditory) information processing must take place ata higher cortical level in a dissociative manner. (Br. J. Anaesth.1993; 71: 629–632)     

Some properties of a nonautonomous deterministic growth model describing the adjustment of the bacterial population to a new environment

Present address: Unilever Research, Colworth Laboratory, Colworth House, Sharnbrook, Bedford MK44 1LQ, UK. Some mathematical properties of a simple nonautonomous deterministicgrowth model are presented. The model describes the lag phaseof bacterial growth as an adjustment of the population to anew environment after inoculation. A useful family of ‘adjustmentfunctions’ is considered and some of its mathematicalproperties are given.     

Signal-Averaged ECG Prior to and Serially After Thrombolytic Therapy for Acute Myocardial Infarction

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7–10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 ± 11.3 ms and 93.4 ± 8.0 ms vs 103.3 ± 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 ± 29.1 μV and 58.6 ± 44.7 μV vs 44.4 ± 35.5 μV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.     

AGGRESSIVENESS, ONSET OF DEPENDENCE, AND TREATMENT OUTCOME IN SOCIALLY WELL-ADAPTED ALCOHOLICS

Current typologies of alcoholism derive from the whole spectrumof afflicted persons. One type is characterized by variablessuch as early onset of dependence, violence, and aggressiveness.In previous research, this has been shown to be correlated withpoorer prognosis. We tested this association in a fairly homogeneoussubgroup of 258 socially rather well-adjusted male inpatients.Aggressiveness was assessed psychometrically. As a group, patientsdid not differ from general population norms. However, age wasnegatively correlated with aggressiveness. Even after takingpatients' age and duration of dependence into account, aggressivenesswas associated with an early onset of dependence and furtheraspects of drinking history, thus confirming results from previoustypology research. Overall treatment outcome after 6 and 12months was quite good, but was not influenced by aggression.     

Interaction Between Accessory Pathways Resulting in Inability to Induce Reciprocating Tachycardia

A 44-year old male with Wolff-Parkinson-White syndrome presented with atrial fibrillation. The patient was found at the electrophysioiogical study to have two accessory pathways, one concealed and the other conducting exclusively in the anterograde direction. After radiofrequency catheter ablation of the anterograde conducting pathway, orthodromic reciprocating tachycardia, which previously could not be induced despite an aggressive protocol, was easily induced. Ablation of the concealed pathway resulted in termination of the tachycardia and suppression of inducibility. We propose that interaction between the two accessory pathways resulted in an inability to induce reciprocating tachycardia.