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Biomedical subjects

R L Reddick

Publications and source records attributed to R L Reddick.

At least 91 records · Page 5Linked to original sources
PubMed1978

Immunoblastic sarcoma of the central nervous system in a patient with lymphomatoid granulomatosis.

A 26-year-old man with lymphomatoid granulomatosis (LYG) was found at postmortem examination to have an immunoblastic sarcoma involving the central nervous system. Residual evidence of LYG was present only in the lungs at autopsy. Studies for intracellular immunoglobulin utilizing the immunoperoxidase technique showed a marked polyclonal reaction in sections of lymph nodes and occasional cells in the cellular central nervous system tumor that stained for intracellular immunoglobulins (IgG, IgM and both kappa and lambda). This case may represent another example of immunoblastic sarcoma occurring in the presence of an abnormal immune state or proliferation.

Adult↗
PubMed1978

Small bowel obstruction as a complication of disseminated varicella-zoster infection.

A 40-year-old woman with Sjögren's syndrome and mixed cryoglobulinemia, treated with corticosteroids, presented with small bowel obstruction temporally associated with cutaneous varicella-zoster (V-Z) infection. At laparotomy a portion of inflamed, necrotic small bowel was resected. Cells in the margin of the lesion exhibited characteristic intranuclear inclusion bodies. This case report emphasizes the multiple organ involvement that can occur with disseminated V-Z infection. Despite the rarity of gastrointestinal involvement, this infection must be included in the differential diagnosis of the acute abdomen in patients with cutaneous vesicles.

Adult↗
PubMed1977

Cutaneous infarction. Manifestation of disseminated mucormycosis.

We describe the second reported case of cutaneous infarction as a manifestation of disseminated mucormycosis. The lesion, which closely resembled ecthyma gangrenosum, occurred in a leukemic patient who was on a regimen of broad-spectrum antibiotics. In this case as in the only other reported case, Mucor pusillus was the cause.

Adult↗
PubMed1975

Characterization of human platelets separated from blood by ADP-induced aggregation.

Separation of platelets from plasma is achieved by adding ADP (final concentration 10-5 M) to platelet-rich plasma and allowing aggregates to form. Aggregates are removed quickly by brief, gentle centrifugation, washed two to three times with 0.9% NaCl (saline), and then incubated for 10 minutes in the presence of apyrase, albumin and calcium. Platelet aggregates deaggregate completely during this incubation period. The platelet suspension is then subjected to 1100g for 12 minutes, gently resuspended in a small volume of saline, and finally diluted with an appropriate medium to the desired concentration. The entire separation procedure requires approximately 30 minutes. Platelets obtained by this procedure are a) comparable in aggregability to the platelet preparations obtained by gel filtration, b) have normal intracellular amounts of ATP and ADP, and c) except for slight dilatation of the surface-connected canalicular system, have normal ultrastructural appearance. When suspended in an appropriate medium, these separated platelets take up serotonin 14-C and subsequently release it in nearly normal quantities when exposed to thrombin, collagen or ADP.

Adenosine Diphosphate↗
PubMed1973

Freeze-etch observations on the plasma membrane and other structures of normal and abnormal platelets.

Human platelets in plasma were subjected to freeze fracture followed by etching. The outer surface of the platelet plasma membrane was exposed by etching but not by fracturing and was clearly identified by use of latex particles as markers. Surface-associated particles, apparently embedded in the plasma membrane, were found to measure from 83 to 332 A in diameter. Similar particles were associated with membranes lining the surface-connected canalicular system and with limiting membranes of storage granules. Fortuitous fractures exposed two inner faces of the plasma membrane, one of which contained greater numbers of surface-associated particles than did the outer surface of the plasma membrane. The second inner face of the plasma membrane contained numerous fibrillar structures measuring up to 770 A in length. Platelets from a congenitally afibrinogenemic patient appeared normal when examined by freeze-etch technics. Normal platelets exposed to a potent antiaggregating agent (REM 10,393) were found to have lost most of the particles associated with the outer surface of the plasma membrane and to have developed numerous defects in this membrane. A possible role for surface associated particles in platelet aggregation was further suggested by the finding that the nonaggregable platelets of two congenitally thrombasthenic sisters were nearly devoid of these structures.

Afibrinogenemia↗
PubMedDate not supplied

von Willebrand factor and occlusive arterial thrombosis. A study in normal and von Willebrand's disease pigs with diet-induced hypercholesterolemia and atherosclerosis.

The thrombotic response of atherosclerotic arteries to stenosis and injury was studied in 14 pigs, eight normal and six with von Willebrand's disease (vWD). Atherosclerosis was produced by feeding a 1% to 2% cholesterol diet for 24 weeks. Both groups of pigs developed severe hypercholesterolemia, greater than five times baseline values. Coronary atherosclerosis was detected in all vWD pigs and in all but one normal pig and was not significantly different between groups. At sacrifice under general anesthesia, a Goldblatt clamp (GC) was positioned around the left anterior descending coronary (LAD) and carotid arteries to produce a stenotic segment, which was pinch-injured with needle holders. A 20 MHz Doppler velocity crystal was placed distal to the GC to detect cyclic flow reductions or permanent cessation of flow velocity indicative of occlusive thrombosis. In the phenotypically normal pigs with diet-induced atherosclerosis, occlusive thrombosis was detected in seven of seven LAD and seven of seven carotid arteries. In atherosclerotic vWD pigs, occlusive thrombosis failed to form in six LAD and 10 carotid arteries (p less than 0.003, Wilcoxon rank sum test). Scanning electron micrographs demonstrated platelet-fibrin microthrombi in both groups of pigs; only phenotypically normal pigs had occlusive thrombi. Von Willebrand factor is essential for the development of occlusive thrombosis and appears to support the progression of a mixed microthrombus to an occlusive thrombus.

Animals↗
PubMedDate not supplied

Coronary atherosclerosis in the pig. Induced plaque injury and platelet response.

The thrombogenic potential of atherosclerotic diet-induced coronary atherosclerotic plaques was investigated in normal swine and in bleeder swine with homozygous von Willebrand disease. Fourteen paired normal and bleeder swine were placed on a 1% cholesterol diet for 1 to 16 weeks. Serum cholesterol was elevated in all animals at sacrifice. Foam cell deposits developed in all major epicardial coronary arteries, and lesions progressed over time from small subendothelial foam cell deposits to fibrous cap lesions that contained foam cells, elastic fibers, collagen, degenerative material, and smooth muscle cells. Balloon catheter injury resulted in platelet deposition, largely in a monolayer or as small platelet clumps devoid of fibrin. Lipid debris was present in injured areas of the subendothelium but did not induce thrombus formation. When the injury involved the media, platelet-fibrin thrombi were formed. Lipid was not present in these thrombi. Morphometric analysis of platelet deposition on ballooned atherosclerotic vessels showed similar numbers of platelets in both phenotypes. However, the attached platelets in bleeder pigs showed significantly less spreading than did those in the normal animals. The results show that injury to intimal foam cell and mixed cellular lesions in coronary arteries of cholesterol-fed swine does not promote the development of platelet-fibrin thrombus formation. In contrast, when the injury extended to the media, mixed thrombi were formed.

Animals↗
PubMedDate not supplied

Smooth muscle cell proliferation in response to endothelial injury in coronary arteries of normal and von Willebrand's disease swine.

The proliferative response of medial smooth muscle cells to balloon-induced endothelial denudation was measured in coronary arteries of normal and von Willebrand's disease swine, a strain of swine with a genetic defect affecting platelet-vessel wall interactions. Animals were sacrificed 48 hours following endothelial injury. Incorporation of a 1-hour pulse label of 3H-thymidine was determined by measuring DNA specific activity. Autoradiography of coronary artery step segments was also performed. The ratio of DNA specific activity in ballooned vessels to that in nonballooned vessels ranged from 1.2 to 26.2. No statistically significant difference in 3H-thymidine incorporation between the two phenotypes was documented (p greater than 0.25). Similarly, DNA incorporation of 3H-thymidine as determined by autoradiography was accelerated to the same degree in ballooned vessels in both phenotypes. The results suggest that von Willebrand factor-mediated platelet activation is not essential for the release of platelet-derived growth factor or that in vivo factors other than platelet-derived growth factor play a significant role in the response of medial smooth muscle cells to acute intimal injury causing endothelial denudation.

Animals↗
PubMedDate not supplied

Development of coronary atherosclerosis in swine with severe hypercholesterolemia. Lack of influence of von Willebrand factor or acute intimal injury.

The development of coronary atherosclerosis in response to acute intimal injury and severe hypercholesterolemia was studied in 18 swine, nine normal and nine with von Willebrand's disease, an inherited disorder affecting platelet-vessel wall interactions. The left anterior descending coronary artery was denuded of endothelium by balloon catheterization, while the circumflex and right coronary arteries served as nonballooned controls. All swine were maintained on a 2% cholesterol diet for 4 months. The extent of atherosclerotic involvement was evaluated from four indices: percent intimal area, percent luminal narrowing, ratio of intimal to medial area, and luminal form. No differences in coronary atherosclerosis were observed between phenotypes in either ballooned or nonballooned vessels, nor were there any differences between ballooned and nonballooned vessels within either phenotype (p greater than 0.05). The major variable affecting coronary atherosclerosis was serum cholesterol. There was a significant positive relationship between serum cholesterol concentration and the extent of intimal lesions (r = 0.62, p = 0.006) that was independent of plasma von Willebrand factor concentration. These findings suggest that severe hypercholesterolemia promotes the development of porcine coronary atherosclerosis through a mechanism(s) that is independent of acute intimal injury or von Willebrand factor-mediated platelet response to injury.

Animals↗