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Biomedical subjects

A Kadish

Publications and source records attributed to A Kadish.

62 records · Page 4Linked to original sources
PubMed1979

Mutagen-induced disturbances in the DNA of human lymphocytes detected by antinucleoside antibodies.

The alkylating mutagens N-methyl-N'-nitro-N-nitrosoguanidine, methyl methanesulfonate, and N-nitroso-methylurea induced immunoreactivity to antinucleoside antibodies in human peripheral blood lymphocytes in vitro. This could also be detected in lymphocytes taken from a patient soon after i.v. administration of cyclophosphamide. The immunoreactivity response, which indicates denatured DNA or DNA single-strand breaks, was scored by immunofluorescent or immunoperoxidase techniques. Examination of blood from 10 normal subjects showed that 32 +/- 4% (S.E.) of resting peripheral blood lymphocytes were immunoreactive to antinucleoside antibodies. We have shown that these naturally occurring immunoreactive lymphocytes are largely accounted for by a subpopulation of thymus-derived lymphocytes bearing the Fc receptor for immunoglobulin M. The presence of these cells did not interfere with the use of peripheral blood lymphocytes for in vitro measurement of additional immunoreactivity caused by alkylating mutagens. The response proved to be dose dependent; up to 90% of lymphocytes could be rendered immunoreactive. Parallel studies with HeLa cells showed a similar dose-response relationship between mutagen action and immunoreactivity. With some agents, the immunoreactivity technique detected effects at lower concentrations than could be detected by HeLa cell survival studies. With N-nitrosomethylurea, measurement of DNA repair synthesis by [3H]thymidine autoradiography showed that in HeLa cells these two parameters of response to DNA damage increased in parallel. Our results provide a new basis for detecting the action of alkylating mutagens on human lymphocytes in vitro or in vivo.

Alkylating Agents↗
PubMed1978

Impairment of cell-mediated immunity in ectodermal dysplasia with aplastic anemia.

A case of ectodermal dysplasia and aplastic anemia is presented in which a cell-mediated immunodeficiency led to a fatal Pneumocystis carinii infection. Elevated levels of IgG, IgA and IgD were present with normal specific antibody titres. A deficient cell-mediated immunity was documented by low T cell numbers, poor in vitro mitogenic responses, negative skin tests and by the histologic finding at autopsy of thymic dysplasia.

Anemia, Aplastic↗
PubMedDate not supplied

Ablative therapy for atrioventricular nodal reentry arrhythmias.

Recent studies in the clinical electrophysiology laboratory have advanced our understanding of the physiologic anatomy of the atrioventricular (AV) junction and have helped direct new curative techniques for the treatment of AV nodal (junctional) reentry. In most patients, it appears that the AV node or the inputs to the AV node that constitute the "slow" pathway are located caudal to the compact AV node and His bundle region near the os of the coronary sinus. In contrast, conduction over the "fast" pathway appears to be located along the anterior tricuspid annulus proximal to the traditional His bundle recording position. This physiologic heterogeneity has allowed the development of curative techniques for AV nodal reentry. The current preferred technique involves ablation of the slow pathway by delivering radiofrequency lesions in the region of the coronary sinus ostium. Although several different localization techniques have been developed, the overall success rate for the procedure developed, the overall success rate for the procedure includes a primary success rate that should be over 95%, a 5% to 10% late recurrence rate, and a complication rate of under 2%. Complete heart block as a complication of slow AV nodal pathway ablation is rate but can occur. The improvements in the results of radiofrequency ablation for the treatment of AV nodal reentry have resulted in the increased use of this procedure clinically. It is now reasonable to offer young patients AV nodal modification as primary therapy for AV nodal reentry and to apply the technique in all age groups to drug-resistant patients.

Animals↗
PubMedDate not supplied

Mechanisms and management of paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia (PSVT) is defined as a regular rapid heart beat, which initiates and terminates suddenly. PSVT may have a variety of electrophysiologic mechanisms, including atrial tachycardia, atrioventricular (AV) nodal reentry, and tachycardia involving an accessory AV connection. Atrial tachycardia may be reentrant or may be caused by abnormal automaticity or triggered activity. AV nodal reentry, in which the reentrant circuit is confined to the AV node or the region around the AV node, is the most common type of PSVT in adults. Orthodromic supraventricular tachycardia is the most frequently found tachycardia in patients with accessory AV connections. During orthodromic supraventricular tachycardia, antegrade conduction occurs via the AV node, and retrograde conduction occurs via an accessory AV connection. Other types of PSVT, including junctional tachycardia, are less common. A definitive diagnosis of the PSVT mechanism usually requires electrophysiologic testing, but clinical and electrocardiographic clues may be present. Understanding the mechanism of PSVT can alter therapy because the response to antiarrhythmic drugs may be somewhat different depending on the PSVT type. In addition, the risks and efficacy of catheter ablation for curing PSVT may differ depending on the PSVT type. A better understanding of PSVT mechanisms, which has developed over the past 20 years, has led to dramatic improvements in therapy.

Catheter Ablation↗
PubMedDate not supplied

Incessant atrial tachycardias in a dog with tricuspid dysplasia. Clinical management and electrophysiology.

In a dog, tricuspid regurgitation due to congenital tricuspid dysplasia resulted in extreme right heart enlargement and right heart failure. Incessant supraventricular tachycardias were present, requiring the intravenous administration of verapamil to reduce the ventricular rate. Oral therapy using a combination of verapamil and quinidine was partially effective in controlling the ventricular rate during the following week. At that time, electrophysiologic studies were performed. They revealed that a succession of several atrial tachycardias with different cycle lengths, including one episode of atrial flutter, was present. Atrial activity was spanning the majority of the cycle length in all these arrhythmias. Epicardial mapping was performed during the atrial flutter. This enabled the detection of a depolarization wave-front traveling counterclockwise from the dorsolateral right atrium toward the right appendage, following the tricuspid valve annulus. No areas of abnormal conduction were detected. Because programmed electric stimulation maneuvers could not be performed, definitive conclusions about the mechanism of the arrhythmia could not be drawn. The two most likely possibilities were circus movement using part of the dilated tricuspid valve annulus as an anatomic barrier or a leading circle type of re-entry.

Animals↗
PubMedDate not supplied

Automatic internal cardioverter defibrillator: a bridge to heart transplantation.

The automatic internal cardioverter defibrillator (AICD) is effective in preventing death in patients with malignant ventricular arrhythmias (VT/VF) refractory to medical therapy. Because of the long waiting period for heart transplantation and the high likelihood of sudden arrhythmic death in this population, this study was undertaken to assess the value of the AICD in patients awaiting heart transplantation who have refractory VT/VF. Fourteen patients awaiting heart transplantation who had a history of VT/VF underwent AICD implantation (10 extrapericardial and four intrapericardial) via median sternotomy. All patients survived the AICD implantation and have either had heart transplantation or await transplantation at present (1 to 24 months after AICD implantation). Twelve of these patients have received a mean of 10 AICD shocks (range, 0 to 32). One patient received 19 shocks in the 24-hour period before transplantation. Two patients have died of progressive heart failure. Five patients have gone on to successful transplantation, and seven patients await heart transplantation with a functioning AICD in place. In conclusion, the AICD represents a new "bridge" to heart transplantation that is well tolerated by these high-risk patients, avoids drug side effects, and is efficacious in aborting sudden death, thereby allowing them to undergo successful heart transplantation.

Actuarial Analysis↗