Publications by authors named "William E Stehbens"

To resolve controversy over umbilical vessels structure, a morphological review was undertaken of the histology of blood vessels in 130 fetal umbilical cords varying in gestational age and the ultrastructure of blood vessels in 6 umbilical cords. Arteries and veins were lined by endothelium. The internal elastic lamina was frequently interrupted when associated with intimal thickening of longitudinally orientated smooth muscle cells.

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Dominant types of viral hepatitis are presently A, B, and C with prophylactic immunization available only for A and B. Hepatitis B and C and human immunodeficiency virus (HIV) infection constitute a worldwide scourge and treatment is far from satisfactory. Each produces severe oxidative stress (OS) and secondary cellular damage of varying severity and, as in toxic hepatitis, progression and regression are dependent on redox balance between oxidation and antioxidation.

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Seromas and prolonged, excessive drainage of serous fluid constitute the most common complications of mastectomy for breast carcinoma. The pathogenesis of this drainage problem is analysed from a pathological perspective and encompasses the role of biomechanical stresses involved in healing. Closed suction drainage delays healing and contributes to the accumulation of serum fluid in the wound.

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Hepatic metabolism of biological toxins, industrial poisons, and medicinal agents involves disturbed hepatic cell biochemistry with augmented generation of reactive oxygen species and free radicals and redox imbalance with secondary damage to proteins, nucleic acids, lipids, and carbohydrates. The xenobiotic hepatotoxicity ranging from a subclinical anicteric state to severe necroinflammatory hepatitis (acute, recurrent or chronic) and cirrhosis depends on the nature, dosage, and duration of exposure to the xenobiotic, the antioxidant defence, and concomitant exposure to other diseases or xenobiotics. Experimental and clinical studies suggest that xenobiotic hepatotoxicity with variable depletion of antioxidants can be avoided or ameliorated by administration of an unusually high dosage of zinc or by a combination of antioxidants above normal daily requirements.

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For a young scoliotic boy the customary "wait and watch" management program for rapidly progressive juvenile idiopathic scoliosis was considered unsatisfactory in view of the poor prognosis. The management program devised was based on the congenital postural induction concept of scoliosis with progression accruing from mechanically induced bioengineering fatigue, cumulative molecular scissions, laxity of ligaments, and secondary bone deformation. A coexisting pelvic tilt with restricted movement of the hip and shoulder joints was overlooked initially.

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Scoliosis, a lateral deviation of the spine frequently associated with rotation, is not a specific disease but a deformity complicating many diseases. Curve progression is the major concern irrespective of the initiating cause. Idiopathic scoliosis is arguably postural in nature and in some subjects develops from intrauterine compression.

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Ubiquitous atherosclerotic changes in fetal and pediatric subjects demonstrate the fundamental importance of repetitive hemodynamic stresses and cannot be explained on the basis of the hypercholesterolemic/lipid hypothesis because serum cholesterol levels at this age lie within allegedly "desirable blood levels." This fact, inconsistent with the lipid hypothesis, renders absurd the widespread dietary restriction of cholesterol and animal fats as prevention of atherosclerosis. Iatrogenic effects of atherosclerosis in humans and its experimental production in herbivores at serum cholesterol levels below infant levels strongly support the "vascular fatige" concept and negate the lipid hypothesis.

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The consistent topography, transmural involvement, and variation in severity and rate of progression in individual atherosclerotic lesions collectively indicate the dominant, primary role of hemodynamics. Specific anatomic configurations, vessels with elevated pressure, high velocity, or disturbed flow and iatrogenic production of accelerated atherosclerosis and its complications in therapeutic venous bypass grafts and arteriovenous shunts point to this role. The morphology and complications are consistent with the loss of cohesion and tensile strength of mural constituents and irreconcilably different from those of cholesterol- or fat-overfed animals and from other metabolic lipid storage disorders.

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