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Biomedical subjects

M A Samuels

Publications and source records attributed to M A Samuels.

At least 19 recordsLinked to original sources
PubMed1993

Comparison of laser phacovaporization using the Er-YAG and the Er-YSGG laser.

OBJECTIVE: To study the interaction of the erbium (Er)-YAG (2.94 microns) and the Er-YSGG (2.79 microns) lasers with the human crystalline lens tissue. METHODS: Fresh human crystalline lens sections were used to measure the photovaporization threshold, rate, and damage zone of the two lasers. RESULTS: We found the photovaporization threshold for the Er-YAG and the Er-YSGG lasers to be 1.4 J/cm2 and 5.5 J/cm2, respectively. At 10 J/cm2, the photovaporization rate is 67.9 microns per pulse for the Er-YAG laser and 18.4 microns per pulse for the Er-YSGG laser. The increased rate of photovaporization as a function of radiant energy for the Er-YAG laser is almost twice that for the Er-YSGG. Damage zones for the Er-YAG laser ranged from 4 to 9 microns compared with 10 to 22 microns for the Er-YSGG. CONCLUSIONS: It is apparent that both lasers can adequately photovaporize human crystalline lens tissue and should be further studied for this purpose.

Cataract Extraction↗
PubMed1993

Neurally induced cardiac damage. Definition of the problem.

Sudden unexpected death is a problem of major importance, but very little is known about its cause. Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. This article discusses the neuroanatomy of the heart and lungs and neurogenic lung and heart disease. The four classes of causes of these abnormalities are catecholamine infusion, stress plus or minus steroids, nervous system stimulation, and reperfusion. These classes are tied together by a common thread, the essential feature of which is sympathetic overactivity with secondary catecholamine toxicity. A unifying hypothesis is proposed to explain all of the forms of sudden death based on the anatomic connection between the nervous system and the heart and lungs.

Cardiovascular Diseases↗
PubMed1993

Cervical bruit.

Explore the source record for details and available documents.

Auscultation↗
PubMed1990

Cerebral toxoplasmosis in patients with AIDS.

Toxoplasma gondii, a previously rare cause of central nervous system infection, has become a major cause of encephalitis in patients with acquired immunodeficiency syndrome. The diagnosis of cerebral toxoplasmosis should be kept in mind when neurologic signs and symptoms develop in patients with AIDS. Patients with positive serology and characteristic lesions on computed tomographic scans should receive two weeks of antitoxoplasma therapy. Biopsy is recommended for patients with atypical presentation, negative serology, progressive clinical deterioration or differential response of lesions to empiric therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Cerebral toxoplasmosis in the acquired immune deficiency syndrome.

We examined the clinical and pathological features of 26 patients who presented with a diagnosis of CNS toxoplasmosis. Patient data was analyzed with respect to demographics, clinical presentation, treatment course and pathology. Patients presented with a wide variety of signs and symptoms. All patients had positive serum antitoxoplasma IgG; ring enhancing lesion(s) were present on all but one brain CT scans. A series of guidelines in the management of CNS toxoplasmosis in AIDS patients are presented. Prior to biopsy, patients with positive serology and characteristic CT scans should receive two weeks of treatment. Biopsy is indicated in those cases with negative serology, atypical presentation, progressive clinical deterioration, or differential response of lesions to empiric therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Sensory form of acute polyneuritis.

A patient presented with severe sensory loss and ataxia with total arreflexia, and elevation of CSF protein with pleocytosis. At autopsy there was extensive lymphocytic infiltration of nerves and posterior roots, sparing the anterior roots. Teased fiber preparation of nerve showed a demyelinating lesion. There were no abnormalities in the CNS. The condition appears to be an acute sensory polyneuritis bearing a close relationship to acute Guillain-Barré syndrome.

Acute Disease↗
PubMed1987

Neurogenic heart disease: a unifying hypothesis.

Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.

Animals↗
PubMed1987

Myocardial contraction band lesions in patients with fatal asthma: possible neurocardiologic mechanisms.

Myocardial contraction band necrosis (MCBN) occurs in catecholamine infusion, central nervous system stimulation, stress, and transient myocardial ischemia with reperfusion. In 4 of 13 children who died with asthma, MCBN was present, suggesting that this cardiac lesion may contribute to the deaths of some asthmatic patients. Two of the 4 patients who had MCBN had not received sympathomimetics intravenously or by an intracardiac route. Therefore, mechanisms other than infusions of large doses of catecholamines are probably involved in production of this cardiac lesion in asthmatics.

Adolescent↗