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Biomedical subjects

R R Smith

Publications and source records attributed to R R Smith.

At least 55 records · Page 3Linked to original sources

Fibroepithelioma of Pinkus. Eccrine duct spread of basal cell carcinoma.

The spread of basal cell carcinoma (BCC) directly into the dermis or down the sides of hair follicles is a common-place pathologic observation. BCC spread via eccrine ducts, which has received less recognition, is the subject of this investigation. We specifically address the question of whether eccrine duct spread accounts for the histologic pattern of the fibroepithelioma of Pinkus (feP) type of BCC. Twenty-five BCC, including 12 feP, five superficial BCC, six ordinary BCC, one BCC of the sole of the foot, and one BCC with prominent hair follicle spread were studied with H&E sections; 11 were immunostained for carcinoembryonic antigen. In ordinary BCC, occasional entrapped eccrine ducts were present. One superficial BCC surrounded the proximal portion of an eccrine duct. The BCC from the sole of the foot showed advanced spread down eccrine ducts; focal obliteration of duct epithelium and lumen was seen, as was transition to strands of solid BCC. Nine of the 12 feP showed one or several eccrine duct foci with tumor strands. These findings suggest that eccrine ducts serve as an initial template in feP and subsequently are replaced by the BCC. However, eccrine duct spread of BCC may occur without necessarily imparting an feP histologic pattern.

Carcinoembryonic Antigen↗

Transcranial Doppler sonography in aneurysmal subarachnoid hemorrhage.

Following subarachnoid hemorrhage (SAH) from an intracranial aneurysm, ischemic deficits related to cerebral vasospasm still account for significant morbidity and mortality. Operative decisions and timing must be based on the presence of vasospasm and other complications of the hemorrhagic period. Transcranial Doppler sonography provides a noninvasive method for evaluating the status of the intracranial arteries following SAH. The method can, with good reproducibility, identify the patient likely to suffer symptomatic vasospasm, outline the progress of the disease, and serve as a guide to therapy. There are inherent errors produced by the anatomy of the intracranial tree and by peculiarities of the disease. Proximal vasospasm, distal vasospasm, defective autoregulation, and distal infarction with hyperperfusion add confusion to the velocity equation. In experienced hands, however, the method correlates well with the angiographic image of the vessels studied.

Humans↗

Prospective, randomized trial of autotransfusion after routine cardiac operations.

To study the effectiveness of autotransfusion of shed mediastinal blood in decreasing the need for homologous blood transfusion in the routine cardiac surgical patient, we prospectively randomized 35 consecutive patients into two groups. The experimental group (n = 18) received autotransfusion for 12 hours after completion of the operative procedure. The control group (n = 17) was treated with standard chest drainage and fluid replacement. Both groups received homologous blood transfusion when the hemoglobin level fell to less than 8.0 g/dL. Student's t test, chi 2 analysis, and multivariate logistic regression analysis were used where appropriate. Packed red blood cells were required postoperatively in 6 of the 17 control and 6 of the 18 autotransfusion patients (p = not significant). Postoperative colloid fluid replacement (excluding autotransfusion fluid) in the autotransfusion group (333 +/- 78 mL; 95% confidence bounds, 168 to 498 mL) was less than in the control group (615 +/- 114 mL; 95% confidence bounds, 372 to 857 mL; p = 0.048). Total homologous blood product exposure tended to be higher in autotransfusion patients (83%) than in control patients (47%) (p = 0.057). Fibrin split products were elevated only in the serum of the autotransfusion patients (p < 0.002). No transfusion-related complications were apparent in either group. Although the sample size is small, autotransfusion of shed mediastinal blood does not appear to decrease the need for homologous blood transfusion in the routine cardiac surgical patient.

Blood Coagulation↗

Strokes in children due to vertebral artery trauma.

Strokes due to vertebral artery lesions are rare in children. We describe three new patients and compare them with the 16 other patients described in the literature. All of these patients are boys. Traumatic vertebral artery lesion at C1-2 level was the most common cause of stroke, and the prognosis for neurologic recovery was good. We suggest that vertebral artery disease be considered in boys with posterior circulation ischemia.

Cerebral Angiography↗

Nonmuscle arterial constriction after subarachnoid hemorrhage: role of growth factors derived from platelets.

Recent studies have shown that myofibroblasts cultured from spastic arteries after subarachnoid hemorrhage (SAH) can produce contractile forces and that cerebrospinal fluid obtained from SAH patients accelerates this contraction. Myofibroblast-populated collagen lattices were used to evaluate the roles of polypeptide growth factors considered to be released from intraluminal accumulated platelets. The myofibroblasts, obtained at autopsy from human cerebral arteries of victims of vasospasm, caused contractile forces by compacting collagen fibrils in the matrix. Transforming growth factor beta 1 (TGF-beta 1) and platelet-derived growth factors aa and bb (PDGFaa and PDGFbb) accelerated this contraction in a dose-dependent manner. In the presence of TGF-beta 1 at 1 or 10 ng/ml, PDGFaa at 10 ng/ml, or PDGFbb at 10 ng/ml, lattice areas were reduced to 69.5 +/- 1.9% (mean +/- standard deviation) (P < 0.001), 63.3 +/- 0.4% (P < 0.001), 66.5 +/- 3.0% (P < 0.01), or 74.4 +/- 1.7% (P < 0.01) of the control on Day 6, respectively. The combination of subthreshold doses of TGF-beta 1 and PDGFaa created a stimulatory effect that appeared to act synergistically. Furthermore, myofibroblast-populated collagen lattices made with cells preincubated with TGF-beta 1 showed more rapid compaction with or without the presence of stimulants such as post-SAH cerebrospinal fluid. These results suggest that, in addition to other possible factors in the post-SAH cerebrospinal fluid, growth factors derived from accumulated platelets may play an important role in arterial constriction caused by nonmuscle components after SAH, by single or multiple mechanisms.

Arteries↗

Experimental chronic compressive cervical myelopathy.

A canine model simulating both cervical spondylosis and its results in delayed progressive myelopathy is presented. This model allowed control of compression, an ongoing assessment of neurological deficits, and evaluation using diagnostic images, frequent electrophysiological tests, local blood flow measurements, and postmortem histological examinations. Subclinical cervical cord compression was achieved in 14 dogs by placing a Teflon washer posteriorly and a Teflon screw anteriorly, producing an average of 29% stenosis of the spinal canal. Four dogs undergoing sham operations were designated as controls. Twelve of the animals undergoing compression developed delayed and progressive clinical signs of myelopathy, with a mean latent period to onset of myelopathy of 7 months. Spinal cord blood flow studies using the hydrogen clearance method showed a significant transient increase in blood flow immediately after compression and a decrease before sacrifice. Somatosensory evoked potential studies indicated progressive deterioration during the period of compression. Magnetic resonance images revealed intramedullary changes. Histological studies showed abnormalities overwhelmingly within the gray matter, including changes in vascular morphology, loss of large motor neurons, necrosis, and cavitation. Axonal degeneration and obvious demyelination were rarely seen. The most profound morphological changes occurred at the site of greatest compression. It is proposed that a momentary arrest of microcirculation occurs during extension of the neck because of loss of the reserve space in the compromised spinal canal. This microcirculatory disturbance is predominant in the watershed area of the cord and mainly affects the highly vulnerable anterior horn cells, leading to neuronal death, necrosis, and eventual cavitation at the junction of the dorsal and anterior horns. Additional supportive evidence of this hypothesis was derived from the literature.

Angiography↗

Solvation effects upon the thermodynamic substrate activity; correlation with the kinetics of enzyme catalyzed reactions. I. Effects of added reagents such as methanol upon alpha-chymotrypsin.

Solvents, detergents, etc., have often been added to the medium to study the kinetics of enzyme action and for binding studies. They have been employed for diverse reasons such as solubilization of substrates or to stabilize an enzyme that was originally membrane bound. Thermodynamic considerations dictate that any added substance, such as methanol, which is present in significant quantity must affect the thermodynamic activities of the enzyme, enzyme-substrate complex, substrate and any other intermediates although cancellation effects may occur in this regard. The influence upon substrate activities is the only one that is easily experimentally accessible. These effects are shown, from the data of Bernard and Laidler, to be large in the case of the alpha-chymotrypsin catalyzed hydrolysis of methylhydrocinnamate. The variation of the Michaelis-Menten constant is quantitatively explainable in terms of the alteration of the thermodynamic activity of the substrate by methanol.

Catalysis↗

Solvation effects upon the thermodynamic substrate activity; correlation with the kinetics of enzyme catalyzed reactions. II. More complex interactions of alpha-chymotrypsin with dioxane and acetone which are also competitive inhibitors.

It is shown that the effects of the addition of various amounts of dioxane and acetone (solvent modifiers) upon the alpha-chymotrypsin-catalyzed hydrolysis of methylhippurate can be explained in terms of three factors. (A) The effects of the above modifiers on the chemical potential of the substrate. (B) The solvent modifiers dioxane and acetone also act as classical competitive inhibitors. The means of sorting out these contributions is presented. (C) The alterations of the chemical potentials or for free energies of the enzyme, enzyme-substrate complex, and/or other intermediates by the added modifiers appear to cancel out with the substrate used here.

Acetone↗

Neuroradiology of intracranial infection.

The ability to detect and differentiate intracranial infection has markedly improved, first with the introduction of computed tomography and, more recently, with magnetic resonance. Enhanced magnetic resonance imaging is the procedure of choice in the evaluation of nearly all intracranial infections. The sensitivity of MR to foci of increased water content, seen in most parenchymal infections, the lack of bone artifact, and the multiplanar capability of MR have led to this preeminence. Computed tomography remains useful primarily in those infections associated with intracranial calcification, such as TORCH syndrome. This article summarizes the most recent CT and MR findings of infection involving the meninges and brain parenchyma.

AIDS-Related Opportunistic Infections↗

Mechanism of action of balloon angioplasty in cerebral vasospasm.

Recent technical advances in interventional neuroradiology have made it possible to dilate cerebral arteries showing vasospasm after a subarachnoid hemorrhage. Although the reported effects of dilatation in clinical cases have been dramatic, few experimental studies of the mechanism of action have been performed. It also is still unclear why dilated arteries rarely show restenosis. Using the scanning electron microscope, we examined changes in the three-dimensional structure of connective tissues in vessel walls after balloon angioplasty. Femoral arteries from cats and middle cerebral arteries from human autopsies were studied. The vessels were dilated in situ with a balloon catheter until the intimal pressure reached 1.5 Wr 3 atm; then they were fixed and digested with 88% formic acid. The specimens were freeze dried and observed under the scanning electron microscope. Normal vessels without balloon dilatation were treated in the same manner and used as controls. The results showed that the normal structure of collagen fibers in the vessel walls was affected significantly by balloon dilatation. Stretched and torn fibers were observed frequently when 3 atm were applied. We concluded that the long-lasting effects of balloon dilatation may be caused by the disruption of connective tissues that proliferate in the vessel wall after a subarachnoid hemorrhage.

Angioplasty, Balloon↗

Accelerated nonmuscle contraction after subarachnoid hemorrhage: culture and characterization of myofibroblasts from human cerebral arteries in vasospasm.

Cell culture lines from human cerebral arteries showing vasospasm after subarachnoid hemorrhage were established from three autopsy cases. Each culture line showed the ultrastructural characteristics of myofibroblasts. Decreased alpha-actin antigenicity, demonstrated using the anti-smooth muscle cell alpha-actin antibody, was observed in cultured cells possessing abundant F-actin. When incorporated into the three-dimensional collagen matrix in vitro, the cultured cells compacted the collagen lattice at a rate equivalent to that of human dermal fibroblasts. Lattice compaction was significantly accelerated by cerebrospinal fluid taken from patients with symptomatic vasospasm. Compaction was completely inhibited by the addition of 10(-6) mol/L verapamil or 100 U/mL heparin. Neither nimodipine (10(-5) mol/L) nor nicardipine (10(-5) mol/L) inhibited compaction, and endothelin (10(-6) mol/L) and potassium chloride (40 mmol/L) had no effect. The morphological change of cells in the collagen lattice suggests that both verapamil and heparin affect cellular motility, filopodial protrusion, and cell attachment. These data suggest that myofibroblasts in human cerebral arteries differ from medial smooth muscle cells and can generate a force rearranging the proliferated collagen matrix present after subarachnoid hemorrhage. This reorganization can contribute to, or be responsible for, sustained vasoconstriction. Consequently, current treatment for vasospasm may need to be reevaluated to include the nonmuscle components in the vessel wall.

Aged↗