Biomedical subjects
D Drachman
Publications and source records attributed to D Drachman.
Recording of pacing stimulus artifacts by endovascular defibrillation lead systems: comparison of true and integrated bipolar circuits.
BACKGROUND: The occurrence ICD undersensing of ventricular fibrillation due to the presence of a pacing stimulus artifact (PSA) is in part related to the amplitude of the artifact recorded on the ICD rate sensing circuit. There is little comparative data regarding PSA amplitude recorded by commercial ICD rate-sensing circuits. PURPOSE: To compare PSA amplitude recorded by commercial endovascular defibrillation leads utilizing integrated or true bipolar sensing circuits. METHODS: Nineteen large (60-120 kg) pigs were utilized. Two different commercial endovascular defibrillation leads were evaluated, each with its distal tip located at the right ventricular apex: (1) Medtronic Transvene; and (2) CPI Endotak. Three different rate-sensing circuits were evaluated: (1) Transvene true bipolar (tip-ring); (2) Transvene integrated bipolar (tip-coil); and (3) Endotak integrated bipolar (tip-coil). Using a separate pacing lead located at the left ventricular apex (n = 19 animals) or right ventricular outflow tract (n = 10 animals), pacing was performed at a pulse width of 0.5 milliseconds at outputs of 1.5, 5 and 10 volts. PSA amplitude was recorded at each output by each circuit. RESULTS: During pacing from the left ventricular apex, at each pacing output voltage the PSA amplitude recorded by the true bipolar circuit (0.6 +/- 0.1 mV at 1.5 volts, 2.0 +/- 0.5 mV at 5 volts, 3.7 +/- 0.8 mV at 10 volts) was significantly smaller than recorded by the Transvene integrated circuit (1.4 +/- 0.3 mV at 1.5 volts, 3.8 +/- 0.7 mV at 5 volts, 4.1 +/- 0.8 mV at 10 volts) or the Endotak integrated circuit (1.8 +/- 0.4 mV at 1.5 volts, 4.2 +/- 1.0 mV at 5 volts, 6.3 +/- 1.8 mV at 10 volts). During pacing from the right ventricular outflow tract, at each pacing output voltage the PSA amplitude recorded by the true bipolar circuit (0.7 +/- 0.1 mV at 1.5 volts, 1.7 +/- 0.4 mV at 5 volts, 4.0 +/- 0.7 mV at 10 volts) was significantly smaller than recorded by the Transvene integrated circuit (1.1 +/- 0.4 mV at 1.5 volts, 3.9 +/- 1.2 mV at 5 volts, 7.5 +/- 1.8 mV at 10 volts) or the Endotak integrated circuit (1.6 +/- 0.7 mV at 1.5 volts, 4.3 +/- 1.7 mV at 5 volts, 7.5 +/- 2.6 mV at 10 volts). For both pacing sites, the PSA amplitude recorded by the two integrated circuits was not significantly different. CONCLUSIONS: For a given pacing output voltage, PSA amplitude recorded by commercial endovascular rate sensing/defibrillation leads is greater when the sensing circuit is integrated than when it is true bipolar. These data may be helpful in planning ICD implantation in patients with previously implanted permanent pacemakers.
Diagnosis and evaluation of dementia.
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Are the associations between Alzheimer's disease and polymorphisms in the apolipoprotein E and the apolipoprotein CII genes due to linkage disequilibrium?
Allele frequencies for polymorphisms in the apolipoprotein E and the apolipoprotein CII genes were determined in subjects of Ashkenazi Jewish origin with late-onset Alzheimer's disease and in unaffected control subjects from the same ethnic group. A significant association was observed between late-onset Alzheimer's disease and the epsilon 4 (112Cys-->Arg) allele of apolipoprotein E; however, no association was detected with apolipoprotein CII. These results suggest that the association with epsilon 4 is probably not due to linkage disequilibrium.
University Hospitals develop benchmarks for patient satisfaction.
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Acetylcholine receptor presentation by B cells using heterobifunctional antibody conjugates.
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Potassium channel blockers potentiate impulse inhibition by local anesthetics.
The ability of local anesthetics to reduce the amplitude of compound action potentials (CAP) of frog sciatic nerve was examined in the absence and presence of agents that selectively block K+ channels. In the presence of lidocaine concentrations that inhibit the CAP by about 20% at low frequencies of stimulation (1 per min, "tonic inhibition"), the addition of the K(+)-channel blocker tetraethylammonium ion (TEA, 12 mM) increased this inhibition by another 15%. Furthermore, the use-dependent inhibition induced by lidocaine at higher stimulation frequencies (5-20 Hz, "phasic inhibition") was markedly enhanced by TEA: at 20 Hz it increased from 35% with lidocaine alone to 63% with lidocaine plus TEA. A comparable potentiation was rendered by 3,4-diaminopyridine (1 mM), a different K(+)-channel blocker. Similarly, phasic inhibition by bupivacaine also was enhanced by TEA. The K(+)-channel blockers alone slightly depolarized the resting membrane, broadened and elevated the CAP, produced no phasic inhibition, and, during repetitive stimulation, resulted in a less negative steady-state repolarization potential than at rest. Both the broadening of CAP and the depolarizing actions of K(+)-channel blockers increased the presence of open and inactivated states of the neuronal Na+ channels, and thereby enhanced the binding of local anesthetic. The inhibitory actions of saxitoxin, a Na(+)-channel blocker that binds equally well to all channel states, were not potentiated by TEA.
Postmastectomy low-grade angiosarcoma. An unusual case clinically resembling a lymphangioma circumscriptum.
A 90-year-old white woman developed a low-grade cutaneous angiosarcoma arising on a chronically lymphedematous extremity 15 years after a radical mastectomy for breast carcinoma. This neoplasm had the clinical appearance of lymphangioma circumscriptum and was characterized by an unusually benign course with a 3-year follow-up.
Absence of duplication of chromosome 21 genes in familial and sporadic Alzheimer's disease.
The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid beta protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.
The genetic defect causing familial Alzheimer's disease maps on chromosome 21.
Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. Several families have been described in which Alzheimer's disease is caused by an autosomal dominant gene defect. The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21. The localization on chromosome 21 provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome. Isolation and characterization of the gene at this locus may yield new insights into the nature of the defect causing familial Alzheimer's disease and possibly, into the etiology of all forms of Alzheimer's disease.
Search for the familial Alzheimer's disease gene.
The application of molecular genetic techniques to the study of autosomal dominantly inherited Familial Alzheimer's Disease may provide a means to determine the chromosomal location of the defective gene causing this form of Alzheimer's disease. Knowledge of the chromosomal location of the defective gene will provide a basis for isolating and characterizing this gene. Preliminary investigations indicate that several candidate genes can be excluded as the site of the defect. Current data also indicate that the defective gene does not reside close to random DNA markers on the distal portion of chromosome 21. Additional DNA markers on the proximal portion of chromosome 21 long arm are currently being investigated.
Hospital social workers and self-help groups.
Self-help has developed into a significant trend in health care, and the relationship between professional services and self-help has begun to be explored. This article describes a survey that investigated hospital social workers' involvement with self-help groups and reports the need for a dual focus on research and clinical training to prepare social workers for the practice challenges presented by the self-help movement.
Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease.
Clinical criteria for the diagnosis of Alzheimer's disease include insidious onset and progressive impairment of memory and other cognitive functions. There are no motor, sensory, or coordination deficits early in the disease. The diagnosis cannot be determined by laboratory tests. These tests are important primarily in identifying other possible causes of dementia that must be excluded before the diagnosis of Alzheimer's disease may be made with confidence. Neuropsychological tests provide confirmatory evidence of the diagnosis of dementia and help to assess the course and response to therapy. The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information become available.
A method for the determination of drug effectiveness in onychomycosis. Trials with ketoconazole and griseofulvin ultramicrosize.
A new method for assessing drug effectiveness in onychomycosis is presented. It is based on the clinical experience when three systemic antifungal drugs (griseofulvin, thiabendazole, and ketoconazole) are used against onychomycosis. These drugs act clinically as a barrier to the invasion of the fungus toward the proximal areas of the nail plate. A monthly quantity of normal nail plate should be produced by a given subject after the administration of an effective dose of the antifungal being tested. This quantity is best measured at monthly intervals, and this in fact reflects the normal monthly nail plate growth for the individual. Although there is a slight variation among individuals, most normal healthy subjects grow 1.5 to 2 mm of nail plate per month from their large toenails and 3 to 4 mm of nail plate per month from their fingernails. Utilizing this quantitative system, ketoconazole and griseofulvin ultramicrosize were compared in the treatment of distal subungual onychomycosis by Trichophyton rubrum. In a double-blind study, sixteen patients were treated. It appears that both griseofulvin and ketoconazole can eradicate the episode of onychomycosis. One-year use of a topical antifungal cream after clinical cure of onychomycosis prevented reinfection in the 12-month follow-up period. The use of ketoconazole in long-term therapy may result in serious side effects and should be considered carefully prior to treatment.
A residential continuum for the chronically mentally ill: a Markov probability model.
The movement of a group of chronically mentally ill clients among various facilities for residential care was described with a Markov probability model. The results of a goodness-of-fit test indicated that the model accurately captured the flow of clients among the state psychiatric hospital, the in-patient units, the community, and three types of group homes. The model was then used to answer several policy-relevant questions about the functioning of the continuum of residential care, such as how often vacancies can be expected to arise and how efficiently clients are progressing along the continuum.
Psychiatric effects of alternate day steroid therapy.
The prevalence of emotional disorder in a total of 72 patients suffering from myasthenia gravis of from peripheral neuromuscular disorders was assessed, using the General Health Questionnaire and Present State Examination. Approximately half the patients were being treated with an alternate day regime of prednisone, receiving high dosage one day and low the next. Emotional disorder was found to be less prevalent among these patients than among patients not on steroids. The significance of the finding is discussed.
Familial inverted choreoathetosis.
We present a family with infantile onset of progressive choreoathetosis. The movements affected the legs predominantly and also impaired gait. No dementia, seizures, or rigidity was noted. Inheritance was autosomal dominant. This new familial movement disorder can be differentiated easily from other hereditary choreas.