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S Milstein

Publications and source records attributed to S Milstein.

66 records · Page 4Linked to original sources
PubMed1985

Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical ablation of the accessory pathway.

The effect of surgical ablation of ablation of atrioventricular accessory pathways on the incidence of atrial fibrillation in patients with Wolff-Parkinson-White syndrome was examined and the results of preoperative electrophysiologic testing were studied to determine factors predictive of outcome. Among 50 consecutive surgical cases, 19 patients were identified with a past history of at least one episode of spontaneous atrial fibrillation documented by electrocardiogram before surgery. The mean number of episodes of atrial fibrillation was 1.97/patient/year during a mean symptomatic period of 6.9 years before surgery. These patients were compared with 19 consecutive patients undergoing surgery during the same time period who had a history of only reciprocating tachycardia. Patients with atrial fibrillation had a significantly shorter antegrade accessory pathway effective refractory period (270 +/- 39 vs 330 +/- 107 msec; p less than .05) and much faster ventricular rates during induced atrial fibrillation (shortest RR interval 219 +/- 73 vs 294 +/- 60 msec, p less than .005; average RR interval 324 +/- 109 vs 405 +/- 127 msec, p less than .01). Patients with atrial fibrillation also had longer PA intervals (47 +/- 13 vs 37 +/- 7 msec; p less than .02). At preoperative electrophysiologic testing, 18 patients with atrial fibrillation had atrial fibrillation induced and 14 sustained the arrhythmia for longer than 10 min. In contrast, atrial fibrillation, although induced in 14 of 19 patients with reciprocating tachycardia, was not sustained in any. Thus electrophysiologic testing suggested that both accessory pathway properties and atrial vulnerability may predispose to atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Diagnostic assessment of recurrent syncope.

The definitive diagnosis of a cardiac arrhythmia as the basis for syncope is made by electrocardiographic monitoring during a syncopal episode. In the absence of this evidence, abnormalities demonstrated by an electrophysiologic study may suggest the etiology of syncope. Cardiac electrophysiologic testing in patients with recurrent syncope should probably be limited to patients with underlying cardiac disease. These patients are at a higher risk for sudden death and have a high incidence of electrophysiologic abnormalities. In particular, ventricular tachycardia may be evoked and specific therapy for this abnormality is associated with remission of syncope. In contrast, electrophysiologic studies in patients with no underlying cardiac disease have a very low yield of abnormal findings in the order of 10-20%, and should be performed only when there are reasons to suspect the presence of arrhythmias. Furthermore, in patients with no underlying cardiovascular disease there is a high spontaneous remission rate of syncope and the late incidence of sudden death is low, and related to the presence of other systemic illnesses. At present, the significance of nonsustained ventricular tachycardia or ventricular fibrillation induced during cardiac electrophysiologic studies in patients with no documented arrhythmias is unknown, and further prospective studies are necessary to define appropriate therapy for these patients. Further investigation is also required to clarify the spontaneous remission rate of syncope, as this information is of vital importance in assessing the success of any therapeutic modality.

Arrhythmias, Cardiac↗
PubMed1982

Resistance of Salmonella typhimurium TA 1535 to O6-guanine methylation and mutagenesis induced by low doses of N-methyl-N'-nitro-N-nitrosoguanidine: an apparent constitutive repair activity.

Salmonella tester strains which are reverted by base-pair substitution mutagens are relatively insensitive to the mutagenic effects of N-methyl-N-nitroso compounds. One reason for this insensitivity is the ability of these strains to withstand low doses of these compounds before they become sensitive to their mutagenic effects. In this report it is shown that mutagenesis induced by treatment of Salmonella typhimurium TA 1535 with N-methyl-N'-nitro-N-nitroso-guanidine (MNNG) in buffer is biphasic with a low sensitivity range at low doses where little mutagenesis occurs, followed by a high sensitivity range whose onset begins after an apparent threshold dose has been exceeded. levels of O6-methylguanine (O6-MeG) in the DNA extracted from the bacteria follow a similar dose-response curve suggesting a dependency of mutagenesis on O6-MeG. In contrast, levels of 7-methylguanine (7-MeG) in the DNA increase linearly with dose. O6-MeG was undetectable at the lowest dose of MNNG whereas 7-MeG was readily detectable. Although such resistance to O6-alkylation has been demonstrated in MNNG- pretreated (adapted) E. coli, it has not been reported in unpretreated cells. Then isolated DNA was treated with MNNG a linear dose-response in the generation of O6-MeG was observed. The lack of O6-MeG in DNA isolated from MNNG treated cells after low doses is attributed to a saturable, constitutive repair activity in the bacteria. An attempt to observe the removal of O6-MeG from the bacteria after exposure to a short challenge dose of N-nitroso-N-methylurea (NMU) followed by a subsequent incubation in buffer was unsuccessful, probably because all the repair occurred within the time necessary to treat and lyse the cells.

Chromatography, High Pressure Liquid↗
PubMed1982

Domenico Cotugno.

Explore the source record for details and available documents.

History, 18th Century↗
PubMed1981

Otosclerosis.

The following is an English translation of an article written by Adam Politzer in 1913. Otologists of that day, concerned with the more urgent and widespread problems of ear infections and their often-fatal consequences, devoted little time to the study of otosclerosis; many dismissed it as yet another post infectious complication of the mucosa or periosteum of the middle ear. Politzer, using the preeminent research tool of the New Vienna School, the autopsy, was the first to establish our current view that otosclerosis is a primary disease of the labyrinthine capsule. The section on clinical diagnosis is valid and useful today. Except for the use of iodine, believed to slow the spread of the illness, Politzer considered all medical and surgical treatment employed at that time, including the primitive stapedectomy, to be futile.

Ear, Inner↗
PubMed1980

The history of mastoid surgery.

Adam Politzer wrote this article on the history of mastoid surgery for inclusion in Volume II of his History of Otology, Enke Verlag, Stuttgart, 1913. Politzer reviews the decades before antibiotics when the simple or complete mastoidectomy was performed in cases of acute mastoiditis in which abscess formation was suspected; such timely surgery after prevented extensive osseous destruction and also often-fatal meningitis and sinus thrombosis. So-called "radical" surgery began when surgeons realized that simple exposure of the antrum was inadequate to control chronic infection involving the middle ear, ossicles, and meatal walls. "Modified radical" surgery evolved from the attempt to preserve hearing, canal plasty from the attempt to prevent postoperative canal stricture. Politzer describes the surgery designed to close the tympanic ostium of the Eustachian tube and the application of skin grafts to the operative sites.

Europe↗