Hydrogen-induced microelectronic capacitor failure in pacemakers

Ceramic chip capacitors used in hybrid microelectronics for cardiac pacemakers are usually highly reliable. However, under certain conditions of capacitor construction, capacitor materials, mounting techniques, and environmental conditions, high failure rates may occur. A specific example is presented in which a ceramic capacitor used in an implanted pacemaker delaminated and failed approximately 30 days after being implanted. The failed capacitor caused a pulse rate rise, but due to circuit design techniques, the rate increase was limited to an acceptable value. The capacitor that failed was from an isolated lot of capacitors that was manufactured using pure palladium plates. The circuit containing this capacitor was hermetically sealed within a titanium case by welding. During the welding, a small amount of hydrogen was released from the titanium which, over a period of 2 to 4 weeks, was absorbed by the palladium plates in the capacitor. By absorbing the hydrogen, the palladium plates exhibit a volumetric expansion of sufficient magnitude to crack and delaminate the capacitor to the point of failure. Subsequently, the recurrence of this failure mode has been avoided by using capacitors containing special palladium alloys that cannot absorb hydrogen. This phenomenon is of interest to pacemaker designers since mercury batteries used in conventional pacemakers generate large amounts of hydrogen and potentially may be responsible for complications when used in conjunction with capacitors containing palladium.     

A simple flotation and McMaster method (author's transl)

A simple and hygienic flotation and McMaster method is described (cf. Fig. 1): The faeces sample (3-5 gm) is mixed with flotation fluid (40-60 ml) in a disposable plastic cup (cup I) and a circular piece of gauze, with a diameter equivalent to twice the height of the cup plus the diameter of its base, is placed over the cup. By a similar cup (cup II), with the bottom cut off and slits made in the side, the gauze is pressed down in cup I. By this procedure the faeces suspension will be filtered through the gauze and appear in cup II. After 10 minutes some drops after transferred from the surface of the filtrate to a slide by means of a test tube, which is dipped to the bottom of the filtrate and quickly moved over to the slide. The optimal procedure was worked out with faeces containing faeces containing eggs of Ostertagia ostertagi. Saturated sodium chloride with 50 g glucose per 100 ml was found to be a suitable flotation fluid for demonstrating eggs of commonly occurring parasites, e.g., trichostronglyids and ascarids. The described flotation technique is more efficacious than the one hitherto employed. The technique is usable also in connection with a McMaster method: 4 gm. faeces are suspended in 56 ml flotation fluid. Immediately following filtration, filtrate is transferred to a McMaster counting chamber by means of a Pasteur pipette.     

Acute hemodynamic interventions shift the diastolic pressure-volume curve in man

Frame-by-frame analysis of angiograms in 16 patients revealed that hemodynamic interventions are capable of producing substantial shifts in the diastolic pressure-volume curve. Angiotensin raises blood pressure and shifts the entire pressure-volume curve up, and nitroprusside lowers blood pressure and shifts the curve down. Indirect measurements of pleural pressure in seven patients (via esophageal pressure) showed that pleural pressure changes were too small to account for these shifts. Analyzing our results in terms of a theoretical pressure-volume equation previously validated in dog studies did not show the observed shifts to be the product of acute changes in the elasticity of the myocardium itself. This same analysis suggested that indirect changes in the external mechanical constraints acting on the left ventricle such as the right ventricular pressure, the pericardium, and perhaps viscoelastic effects related to changes in filling rate account for the pressure-volume curve shifts with intervention. The fact that one cannot in general relate a specific volume to a given pressure in the face of hemodynamic interventions calls into question the use of end-diastolic pressure interchangeably with end-diastolic fiber length when interpreting systolic events in terms of the Frank-Starling mechanism.     

Rancinamycins I, II, III and IV structural studies

Rancinamycins are secondary metabolites produced by Streptomyces lincolnensis in a sulfur-depleted culture medium. The structures (except stereochemistry) of the main components of the rancinamycin-complex were determined by the use of IR, UV, PMR, and CMR spectra.     

Choroidal neovascular membrane in Best's vitelliform macular dystrophy

The right eye of a 9-year-old white boy with Best's vitelliform macular dystrophy had an intact egg-yolk lesion and a retinal pigment epithelial defect superiorly, suggesting an early pseudohypopyon stage. The disruptive phase of the left eye showed subretinal hemorrhages, a "signet ring," and a subretinal neovascular membrane.     

Cells of origin of entorhinal cortical afferents to the hippocampus and fascia dentata of the rat

The pathway from the entorhinal cortical region to the hippocampal formation has previously been shown to be comprised of two sub-systems, one of which projects predominantly to the ipsilateral fascia dentata and regio inferior of the hippocampus proper, and a second which projects bilaterally to regio superior. The goal of the present investigation was to determine if these two pathways might originate from different cell populations within the entorhinal area. The cells of origin of these entorhinal pathways were identified by retrograde labeling with horseradish peroxidase (HRP). Injections which labeled the entorhinal terminal fields in both the fascia dentata and regio superior resulted in the retrograde labeling of two populations of cells in the entorhinal area. Ipsilateral to the injection, HRP reaction product was found in the cells of layer II (predominantly stellate cells) and the cells of layer III (predominantly pyramidal cells). Contralateral to the injections, however, the reaction product was found almost exclusively in the cells of layer III. With selective injections of the entorhinal terminal field in regio superior, only the cells of layer III were labeled, but these were labeled bilaterally. Selective injection of the entorhinal terminal field in the fascia dentata, however, resulted in the labeling of cells of layer II, but not of layer III, and these cells of layer II were labeled almost exclusively ipsilaterally. A very small number of labeled cells in layer II were, however, found contralateral to the injection as well. No labeled cells were found either in the presubiculum or parasubiculum following injections of the hippocampal formation. These cell populations were found capable of retrograde transport of HRP, however, since cells in both presubiculum and parasubiculum were labeled following HRP injections into the contralateral entorhinal area. These results suggest that the projections to the fascia dentata originate from the cells of layer II, while the projections to regio superior originate from the cells of layer III of the entorhinal region proper. The very slight crossed projection from the entorhinal area to the contralateral area dentata probably originates from the small population of cells in layer II which are labeled following HRP injections in the contralateral area dentata.     

Adrenergic receptors mediating depolarization in brown adipose tissue

Adrenergic receptors mediating depolarization in in vitro neonatal rat brown adipose tissue (BAT) have been characterized by use of adrenergic agonists and antagonists. Releasable endogenous catecholamine was present in BAT as demonstrated by tyramine- and 1,1-dimethyl-4-phenylpiperazinium iodide- (DMPP) induced depolarization in BAT from normal rats and its absence when BAT from reserpinized rats was used. In BAT from reserpinized rats l-norepinephrine, l-phenylephrine, and l-isoproterenol all similarly depolarized the bronw adipocytes over the concentration range of 10(-8) to 10(-6) M with a maximal depolarization of about 25 mV. Dopamine and d-norepinephrine were more than 100 times less potent. The beta-adrenergic blocker propranolol competitively inhibited isoproterenol-induced depolarization, whereas the alpha-adrenergic blackers, phentolamine and phenoxybenzamine, inhibited the phenylephrine-induced depolarization with much smaller inhibitory effects on the isoproterenol-induced depolarization. Both phenylephrine and isoproterenol elicited transient depolarizations when briefly added to the bathing medium while continuously recording from the same cell. Both the agonist and antagonist studies are interpreted as indicating the presence of both alpha- and beta-adrenergic receptors on BAT cells which mediate catecholamine-induced depolarization.