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Biomedical subjects

Francis Robicsek

Publications and source records attributed to Francis Robicsek.

13 recordsLinked to original sources
PubMed2002

Cause of degenerative disease of the trileaflet aortic valve: review of subject and presentation of a new theory.

Risk factors for both atherosclerotic aortic wall disease and degenerative disease of the trileaflet aortic valve are very similar if not identical. This correlation grows even stronger as the person advances in years. Because of this, it is the prevailing view that sclerosis of the trileaflet aortic valve, unless previously affected by septic or rheumatic endocarditis, is a disease similar in origin to sclerosis of the aortic wall, ie, degenerative aortic valve disease is arteriosclerosis of the aortic valve. Our studies challenge these views. The aortic valve is a functional assembly composed of the three cusps, corresponding sinuses, and the sino-tubular junction, characterized not only by morphologic features but also by its functional properties, which together create an environment that is optimal for distribution of diastolic pressure load and assures proper and timely valve opening and closure. Our more recent experiments also demonstrate that loss of aortic wall compliance at the level of the sinuses leads to significant stress-overload on the aortic leaflets and it is likely to start a chain of events, which begins with minor changes in their microstructure, then continues in more evident sclerosis, and finally ends in gross distortion or calcification of the cusps. The loss of the "pull-and-release" process may also play a part in disintegration of bioprosthetic valves and in degeneration of native aortic valves encased in noncompliant prostheses.

Aging↗
PubMed2002

Poland's syndrome revisited.

Poland's syndrome is a rare congenital anomaly characterized by unilateral chest wall hypoplasia and ipsilateral hand abnormalities. Literary data suggest its sporadic nature. The prevailing theory of its cause is hypoplasia of the subclavian artery or its branches, which may lead to a range of developmental changes. The incidence of Poland's syndrome varies between groups (male versus female patients, congenital versus familial cases, and so on) and ranges from 1 in 7,000 to 1 in 100,000 live births. Cases of Poland's syndrome associated with leukemia, carcinoma of the hypoplastic breast, and other conditions, confirm the relationship between developmental defects and tumors, and require oncologic awareness. Various manifestations, age, and gender require different surgical approaches. Our experience, which includes 27 patients (15 male, 12 female), 20 of whom (12 male, 8 female) underwent operation, suggests that the repair should be done in two stages in children and in a single stage in adults. Reconstruction and/or stabilization of the aplastic ribs may be achieved using bone grafts or prosthetic mesh. Muscle flaps and breast implants may be used to correct muscle deficiency and breast hypoplasia and to help achieve a complete cosmetic repair.

Adult↗
PubMed2002

Changes in the preserved heart that limit the length of preservation.

BACKGROUND: The variability in donor heart viability following preservation is well known and very dependent on the animal model used and the methods of preservation. Using hypothermia (2 to 4 degrees C) with the University of Wisconsin solution and microperfusion (3 microl/g/min) myocardial functional recovery after reperfusion is 50% to 60% after 18 hours of preservation. Many investigators have found the 18-hour preservation barrier for functional recovery of the heart with different experimental protocols. In previous studies, we have found in normothermic global ischemia that with necrosis there was a significant amount of apoptosis. It was therefore the purpose of this study to investigate the importance of apoptosis in heart preservation and determine if this cellular disruption plays a part in limiting heart viability during recovery from preservation. METHODS: Using a heterotopic heart transplant model, myocardial function (end-systolic elastance), high energy phosphate changes, metabolic substrate utilization, electron microscopy to determine degree of injury, and histologic changes that included apoptosis and lamin B(1) analyses were conducted on canine hearts preserved for 18 hours and reperfused for 6 hours. The changes were compared with a control group with no preservation. RESULTS: The 18-hour preserved heart regained approximately 50% to 60% of its original function, with significant decreases in adenosine triphosphate, no irreversible cellular changes (necrosis), and a 6% to 8% increase in apoptotic myocytes with a concomitant 8% decrease in lamin B(1). CONCLUSIONS: Preserved hearts can be maintained for approximately 12 hours with functional recovery near normal. However, approaching 18 hours, there is an attenuated functional response which may be related to the to development of apoptosis.

Animals↗