Salivary oestriol in normal and abnormal pregnancies

Summary. Profiles of daily salivary oestriol concentrations throughout the third trimester of pregnancy have been constructed for 14 normal and 11 abnormal pregnancies. Day-to-day variations were significantly higher than those reported for unconjugated oestriol in plasma or serum. A sustained decline in salivary oestriol concentrations was observed in one pregnancy in which intrauterine death occurred. Sustained falls were also observed in two pregnancies in which a healthy infant was born at term. In all other patients a normal salivary oestriol profile correlated with a favourable outcome. Salivary oestriol measurements provide similar information to plasma unconjugated oestriol measurements while offering the advantages of a simple, non-invasive sample collection procedure.     

THERAPEUTIC STUDIES IN OSTEOPETROSIS

Four cases of osteopetrosis, with manifestations within the first months of life, are presented. The first two cases were siblings. One of them received no therapy, the other 12 blood transfusions and antibiotics. Therapy had no influence on the thrombocytopenia and haemolytic process in Case 2, and he developed rachitic-like changes and a decrease in serum calcium during hospitalization. Both these two siblings died at the age of 5 months. The last two cases have been on prednisone therapy for 21 and 14 months, respectively. Case 3 is now doing well on prednisone, 7.5–10 mg every other day. Her mental and stato-motoric development has so far been normal. Optic nerve decompression was performed in March 1968, and the eye on which the operation was performed still retains some vision. Case 4 was started on steroids when he was about 3 months older than Case 3. Splenectomy had to be performed due to high prednisone requirements, and he still needs prednisone, 15 mg every other day. He seems, unfortunately, to be blind and slightly retarded. Heparin seems to be of no practical value in this disorder. Cellulose phosphate therapy resulted in impaired calcium absorption. The resulting hypocalcemia seems, however, to have very little, if any, effect on the underlying disease.     

Gross and Microscopic Changes Associated with a Nonthoracotomy Implantable Cardioverter Defibrillator

The pathology associated with an invesrigational transvenous defibriliating and sensing lead is described. The lead system had delivered a total of 865 J from the time of implantation to the time of patient death from a noncardiac cause 7 months after implantation and 1 month after his last defibrillator shock. There was mild, superficial fibrous thickening on the endothelial surface of the superior vena cava adjacent to the proximal spring electrode, which did not extend into the vessel wall. The distal portion of endocardial lead was embedded in the interventricular septum near the apex of the right ventricle, surrounded by fibrous thickening, and partially covered by endocardial tissue. Microscopically, there was a thick bed of fibrous connective tissue surrounding the lead with extensive interstitial fibrous connective tissue radiating into the adjacent myocardium. Since this pattern is different from the more generalized fibrotic scarring produced by myocardial infarction, we speculate that the mechanism for the observed interstitial fibrosis is replacement fibrosis following acute myocyte injury that resulted from prior defibrillator shocks and possibly from the trauma produced by the lead compressing adjacent myocardium during systole. Potential effects on device efficacy of these fibrotic changes at the bioelectric interface include their representing a new arrhythmia substrate, the possibility that fibrosis could increase both defibrillation and pacing thresholds, and that the inflammatory reaction may cause deterioration of intracardiac electrograms and interfere with sensing and tachycardia recognition.     

Effectiveness of community participation in vector-borne disease control

Vector-borne diseases continue to represent a major public healththreat in Latin America. Although vertical programmes that reliedon large teams of workers were successful in stopping or significantlyreducing transmission of malaria, yellow fever and Chagas' diseasein many countries earlier in this century, they have recentlybeen less effective due to a variety of reasons, including thehigh cost of labour and insecticides. Although participatoryapproaches to the control of disease vectors appear to havemany advantages, they have been difficult to implement due toa number of historical, social and cultural factors which arepresent in Latin America. Taking Aedes aegypti control programmesas an example, it is shown that for community participationto work, there must be willingness to define the form participationwill take in consultation with the community, and commitmenton the part of local governments to addressing local concerns,such as difficulties in obtaining good quality drinking water.     

Ventricular Output Failure in a DDD Permanent Pacemaker Associated with Increased Atrial Output

Previous reports have described the occurrence of ventricular autput failure in a permanent DDD pacemaker system related to an increase in the atrial output in the presence of low atrial lead impedance (Medtronic Synergyst®/Synergyst II®). This phenomenon is seen exclusively following atrial paced events and may potentially lead to significant bradyarrhythmia or ventricular asystole in a pacemaker dependent patient. We describe the occurrence of analogous behavior in a Medtronic Symbios® 7006 generator.     

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)