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D Aarons

Publications and source records attributed to D Aarons.

At least 19 recordsLinked to original sources
PubMed1995

Research ethics.

This article reviews the ethical requirements for research. The ethics of human experimentation are informed by the basic principles of beneficence, justice and respect for persons. The principle of beneficence requires that a research protocol present a favourable risk/benefit ratio to subjects. Justice demands that the burden and benefits of research be equitably distributed. Respect for persons entails an obligation both to obtain informed consent from research subjects and to protect those who are unable to consent from the risks of research. The fundamental tenet of research ethics is a prior review by a panel of peers. This article argues for the establishment of Research Ethics Committees across the Caribbean to ensure that clinical research conforms to the highest scientific and ethical standards.

Beneficence↗
PubMed1992

The automatic implantable cardioverter-defibrillator. Long-term clinical experience and outcome at a hospital without an open-heart surgery program.

From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.

Adult↗
PubMed1992

Competition between zonae pellucidae and a proteinase inhibitor for sperm binding.

Murine sperm bind a proteinase inhibitor of seminal vesicle origin at ejaculation. The inhibitor binds in the acrosomal region of the sperm head and is removed during in utero or in vitro incubation. Adding inhibitor to sperm reduces their ability to bind zonae, while adding the purified inhibitor binding site to cumulus-free, zona-intact oocytes reduces the ability of the oocytes to bind sperm. Immuno-aggregation of the inhibitor binding site results in exocytosis of the acrosome. These observations suggest that the inhibitor binding site may participate in zona binding and the acrosome reaction. If the inhibitor binding site binds both the zona and the seminal inhibitor, then these components should compete with each other for that site on the sperm. We show that purified seminal inhibitor, as well as other proteinase inhibitors, block zona-induced acrosome reactions. Likewise, zona glycopeptides block inhibitor/anti-inhibitor-induced acrosome reactions in a concentration-dependent fashion. The inhibitor/anti-inhibitor-induced acrosome reaction is sensitive to pertussis toxin and proteinase inhibitor and thus is similar to zona-induced reactions. These findings support the suggestion that the trypsin inhibitor binding site on the head of the sperm functions to insure sperm-zona binding and induction of the acrosome reaction.

Acrosome↗
PubMed1992

Role of monoclonal antibody J-23 in inducing acrosome reactions in capacitated mouse spermatozoa.

A monoclonal antibody (J-23) to the 15 kDa component on the sperm head, the acceptor, which functions in zona binding, was shown to induce the acrosome reaction in capacitated cells, but not in fresh cells. The antibody recognized its epitope in the acrosomal cap region of fresh spermatozoa and in the equatorial region on washed and capacitated spermatozoa. However, equatorial expression did not depend on the acrosome reaction, since washing fresh spermatozoa increased the percentage with equatorial fluorescence, but did not increase the percentage with reacted acrosomes. The data indicate that the acrosome reaction can be induced in capacitated spermatozoa in the absence of zona glycoproteins.

Acrosome↗
PubMed1991

Acrosome reaction induced by immunoaggregation of a proteinase inhibitor bound to the murine sperm head.

ZP3, a glycoprotein of the murine zona pellucida, functions both to bind acrosome intact sperm and to induce the acrosome reaction. Solubilized whole zonae as well as purified ZP3 are able to induce acrosome reactions in capacitated sperm. Pronase digests of whole zonae yield glycopeptides that bind to sperm but are unable to induce acrosome reactions. However, immunoaggregation of these glycopeptides results in the exocytosis of the acrosome in the majority of treated sperm. The data suggest that ZP3 triggers the acrosome reaction by the aggregation of ZP3 binding sites on the sperm head. If aggregation of ZP3 binding sites is important in the induction of the acrosome reaction, then it may be possible to induce the acrosome reaction in the absence of zona by immunoaggregation of the sites. This presentation deals with the immunoaggregation of a proteinase inhibitor of seminal vesicle origin (SVI) that binds to a site on the sperm head known to participate in zona binding. We show that capacitated murine sperm, pretreated with the SVI, will acrosome react, as determined by Coomassie brilliant blue staining, when incubated with rabbit antiinhibitor antiserum (anti-SVI). The percentage of SVI-treated sperm displaying an acrosome reaction is dependent on the concentration of the immune serum. Sperm stain positive for intact acrosomes when anti-SVI Fab fragments or normal rabbit serum is substituted for the immune serum. However, when capacitated sperm, treated with both SVI and anti-SVI Fab fragments, are incubated with goat antirabbit IgG, the majority of sperm acrosome react. The data suggest that the aggregation of SVI bound to the sperm surface, in the absence of zona glycoproteins, is sufficient to induce the acrosome reaction.

Acrosome↗
PubMed1991

Sudden bradyarrhythmic death in patients with the implantable cardioverter-defibrillator: report of two cases.

Two cases of sudden bradyarrhythmic death necessitating cardiopulmonary resuscitation in patients with the automatic implantable cardioverter-defibrillator are described. One patient had sudden bradyarrhythmic death while being monitored in the hospital. This patient could not be resuscitated and represents the first reported sudden cardiac death secondary to bradyarrhythmia in a patient with the automatic implantable cardioverter-defibrillator. The second patient had an out-of-hospital sudden death followed by probable cardioverter-defibrillator discharge, leading to complete heart block with escape ventricular rhythm necessitating immediate temporary pacemaker insertion. These cases highlight the need for bradycardia back-up pacing and event monitoring in the newer tachyarrhythmia management devices.

Aged↗
PubMed1991

Ventricular pacing threshold and time to capture postdefibrillation in patients undergoing implantable cardioverter-defibrillator implantation.

To assess the effect of defibrillation and amiodarone on ventricular pacing threshold and time to capture in patients undergoing automatic implantable cardioverter-defibrillator (AICD) implantation, 28 patients were prospectively evaluated. The patients were entered into one of two protocols: Ia--epicardial ventricular pacing threshold measured at baseline (preventricular fibrillation induction) and 10 and 60 seconds postdefibrillation with 20 J, or Ib--two fibrillation-defibrillation sequences were performed 3 minutes apart and ventricular pacing thresholds were measured for each sequence at baseline and at 10 and 60 seconds postdefibrillation with 20 J. Ten patients also underwent asynchronous pacing at 1.1 times baseline threshold during ventricular fibrillation with measurement of time to capture postdefibrillation. All patients were randomly assigned to receive either amiodarone or no antiarrhythmic drug therapy. Ventricular fibrillation was induced with AC (applied for 1-2 seconds), and standard epicardial bipolar and epicardial patch electrodes of the AICD were used for pacing and defibrillation, respectively. Ventricular pacing threshold at baseline, 10 seconds, 60 seconds, and 3 minutes postdefibrillation did not differ significantly. There were no significant differences in patients with or without amiodarone therapy. Furthermore, there was no transient loss of ventricular capture postdefibrillation or significant difference in time to capture with amiodarone (less than or equal to 2 seconds). We conclude that following internal defibrillation with 20 J: (1) ventricular pacing threshold at 10 seconds, 60 seconds, and 3 minutes were not significantly different from baseline with one or two fibrillation-defibrillation sequences, (2) time to capture was short, and (3) there was no significant difference in no drug versus amiodarone. These findings have direct clinical importance in considering device therapy with both pacing and defibrillating capabilities.

Amiodarone↗
PubMed1991

Anxiety and depression in patients with life-threatening ventricular arrhythmias: impact of the implantable cardioverter-defibrillator.

In order to assess the psychological responses to the automatic implantable cardioverter-defibrillator (AICD), 18 patients with a history of life-threatening ventricular arrhythmias were requested to complete the Spielberger State-Trait Anxiety Inventory and the Beck Depression Inventory. The patients were divided into three groups of six and matched for age, sex, underlying cardiac disease, ejection fraction, and NYHA Functional Classification. Group I had experienced conscious discharges from the AICD, group II had the AICD but without discharges, and group III without the AICD were treated with antiarrhythmic medications alone based on electrophysiological guided testing. Patients with the AICD were also requested to complete a questionnaire directed specifically at their experiences with the AICD. All of the 18 patients completed the study responses and results were analyzed by blinded review. There were no significant differences in anxiety and depression scores in the three groups studied, nor any significant differences in responses to the questionnaire in group I versus group II. One patient in group I reported experiencing adverse psychological responses to the AICD. Although there appears to be no significant differences in psychological responses as a result of the AICD implantation in patients with life-threatening ventricular arrhythmias, further study with larger patient groups is needed to identify and support patients who may develop adverse responses to the AICD.

Affect↗
PubMed1991

Predictors of first discharge and subsequent survival in patients with automatic implantable cardioverter-defibrillators.

BACKGROUND: Two hundred eighteen patients were evaluated in a two-phase approach (time to first appropriate discharge, survival after discharge) to identify factors that may be related to maximal benefit derived from use of an automatic implantable cardioverter-defibrillator (AICD). METHODS AND RESULTS: One hundred ninety-seven patients survived implantation of AICD, with or without concomitant cardiac surgery. One hundred five patients had an AICD discharge associated with syncope, presyncope, documented sustained ventricular tachycardia or fibrillation, or sleep at 9.1 +/- 11.1 months after implantation. Patients survived 23.8 +/- 18.0 months after AICD discharge. Left ventricular dysfunction (p = 0.008 for ejection fraction less than 25%) was associated with earlier AICD discharge and shortened survival after AICD discharge (p = 0.008 for ejection fraction less than 25%; p = 0.01 for New York Heart Association functional class III and IV). beta-Blocker administration (p = 0.006) and coronary bypass surgery (p = 0.06) were associated with later AICD discharge. Coronary bypass surgery (p = 0.035) but not beta-blockers was associated with more prolonged survival after AICD discharge. CONCLUSIONS: These data suggest that a relatively easy algorithm can be applied to predict which patient will benefit most from AICD implantation.

Electric Countershock↗
PubMed1991

The automated implantable cardioverter.

The automatic implantable cardioverter defibrillatory (AICD) is becoming the treatment of choice for patients with ventricular tachycardia and ventricular fibrillation. The widespread use of the AICD is requiring nurses in a variety of settings to become familiar with the device and device-patient interactions. This article attempts to define specific issues and nursing interventions relative to the AICD.

Aftercare↗
PubMed1985

Competition between seminal and exogenous proteinase inhibitors for sites on murine epididymal sperm.

Sixteen proteinase inhibitors were tested for their ability to compete with the natural seminal inhibitor for binding to the surface of murine epididymal sperm. The most effective competitors, 4-methylumbelliferyl-p-quanidinobenzoate (MUGB) and p-nitrophenyl-p-guanidinobenzoate (NPGB), are also effective inhibitors of both murine acrosin and in vitro fertilization of mouse gametes. The data support the suggestion that the inhibition of fertilization by these inhibitors may be effected by their action on the sperm surface rather than binding to enzymes located within the acrosome. Since the surface acceptor molecule recognizes a number of inhibitor types, as well as substrates for such enzymes as trypsin and acrosin, the acceptor's binding site may be similar to the active site on the enzyme.

Animals↗