Search PubMed⌕ Search

Biomedical subjects

S K Peng

Publications and source records attributed to S K Peng.

65 records · Page 4Linked to original sources

Familial amyloid polyneuropathy.

Amyloid fibrils were isolated from the myocardium of two patients with familial amyloid polyneuropathy. The solubilized amyloid fibril whole protein shared immunologic determinants with normal human serum prealbumin (transthyretin), but revealed subtle differences on immunoelectrophoresis and radial immunodiffusion. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, amyloid fibril whole protein was resolved into numerous bands that reacted with antitransthyretin on immunoblots. The whole protein also contained peptide fragments of fibronectin, but was devoid of amyloid P protein. An antiserum raised against the whole protein was suitable for immunocytochemistry of amyloid in paraffin sections. In contrast, commercial antitransthyretin, raised against the intact tetrameric protein failed to react with tissue amyloid. Immunochemical and immunocytochemical results support the concept that familial amyloid polyneuropathy with cardiomyopathy is due to infiltration of susceptible tissues by an anomalous transthyretin.

Aged↗

Disseminated coccidioidomycosis with rapid progression to effusive-constrictive pericarditis.

This case reports coccidiomycosis presenting as pericarditis with tamponade rapidly progressing to effusive-constrictive pericarditis and death over 72 hours. Coccidiomycosis pericarditis is a rapidly progressing disease requiring early and complete pericardiectomy to avoid the hemodynamics of constriction. We illustrate the use of echocardiography in this case and demonstrate the histopathology. We review the literature and discuss therapy and management. Coccidiomycosis is often clinically unsuspected and unrecognized by the health care worker unfamiliar with the disease process.

Adult↗

A canine iliac artery occlusion model.

This report describes an occlusive canine iliac artery model for use in experimental angioplasty procedures. Lesions were induced by overdistending and breaking the internal elastic lamina of the artery and implanting a 2-cm long occlusive collagen plug. The collagen plug diameter was varied to fit the iliac artery and caused immediate bilateral iliac occlusions. Histology of the lesions at 9 and 14 days (n = 2) showed that the lumen was filled with a mixture of fresh thrombus and collagen pad material (more collagen than thrombus) with focal disruptions of the internal elastic lamina. At 36 days (n = 2) the lumen was obliterated with a mixture of organizing thrombus and collagen pad material (more organizing thrombus than collagen). At 60 (n = 4) and 80 (n = 8) days the collagen pad had been completely replaced with organizing thrombus consisting of collagen fibers and hemosiderin-laden macrophages with persistent focal disruptions of the internal elastic lamina. These initial data demonstrate the ability to create fibrotic arterial occlusions in as short a time as 60 days and to provide a practical model to study methods for treating localized peripheral vascular occlusive disease.

Animals↗

In vivo study of a high-porosity polytetrafluoroethylene graft: endothelialization, fluid leakage, and the effect of fibrin glue sealing.

Standard polytetrafluoroethylene (PTFE) grafts (30-microns internodal distance, ID) (ST grafts), high-porosity PTFE grafts (90 microns ID) (HP grafts), high-porosity PTFE grafts preclotted with autogenous blood (BHP grafts), and high-porosity PTFE grafts presealed with fibrin glue (FHP grafts) were implanted in both common carotid and femoral arteries of 18 dogs. Of the three high-porosity groups, the FHP graft showed the shortest bleeding time. Seromas and/or hematomas occurred as follows: ST grafts 1, HP grafts 7 (P < .05 vs ST), BHP grafts 5 and 2 with FHP grafts. Fibrin glue was observed in all histological sections of 1-week samples, but by 4 weeks it was almost totally absorbed. No endothelialization (ET) was measurable at 2 weeks. By 4 weeks ET extended for a short distance from each anastomosis and there were no significant differences between the four graft groups. At 18 weeks, the HP, BHP, and FHP grafts showed a significant increase in ET compared with the ST graft (P < .01) but there were no significant differences between the three types of high-porosity graft. The differences in patency rates and neointimal thicknesses did not reach statistical significance. High-porosity PTFE grafts showed superior endothelialization in dogs; however, the enlarged ID of PTFE grafts increased intraoperative bleeding and postoperative seroma formation. Fibrin glue sealant controlled bleeding through the graft wall without affecting graft healing, but its sealant effect was not enough to prevent late fluid leakage.

Animals↗

Eccentric iliac artery stenosis: a canine model for angioplasty.

A canine model was developed to induce eccentric iliac artery stenosis. Lesions were induced by exposing the medial aspect of the right and left common iliac arteries in four animals to direct argon laser energy (LA). A 2.5-mm diameter side-firing laser probe was used to deliver 10 W of power in 5-s intervals. Twenty-five pulses were delivered over a 5-cm length of artery with an approximate spot size of 0.8 mm2. Selected arteries (n = 2, LA + Ca) were injected in the same laser injury site with calcium chloride (10% solution). Injections were accurately accomplished using an angioscopically guided guidewire/needle device. In all cases, the internal elastic lamina was broken with focal disruptions of the media. At 9 and 14 days, the LA (n = 3) and LA + Ca vessels (n = 1) had minimal stenoses (< 5% area reduction). These vessels contained edematous media with replacement of necrotic smooth muscle by fibrous tissue. At 23 days, the LA (n = 1) and LA + Ca (n = 1) vessels contained 22% and 33% luminal reductions, respectively, with moderate neointimal proliferation and no evidence of calcification. At 56 days the LA vessels (n = 2) contained 30 and 42% luminal area stenoses with marked neointimal hyperplasia. This preliminary data suggests that controlled arterial wall injury with LA irradiation can induce eccentric fibrointimal lesions in a canine model.

Angioplasty↗

The role of cholesterol oxidation products in the pathogenesis of atherosclerosis.

Cholesterol undergoes spontaneous autoxidation, leading to the production of potentially atherogenic oxidation derivatives. When 25-hydroxycholesterol (25-OH) or cholestane-3 beta, 5 alpha, 6 beta-triol (triol) was injected intravenously into rabbits, the aortic surfaces showed numerous balloon-like protrusions and crater-like defects indicative of endothelial damage. Alterations in membrane function caused by these cholesterol oxides could be the mechanism for their cytotoxic effect. Carrier-mediated hexose transport by cultured rabbit aortic smooth muscle cells, measured using 2-deoxyglucose, was reversibly inhibited by triol within one hour. A membrane-bound enzyme, 5'-nucleotidase, was inhibited after 24 to 48 hrs incubation with either 25-OH or triol. Endocytosis was also significantly inhibited by both 25-OH and triol. Depletion of membrane cholesterol content by the cholesterol oxides could account for the membrane functional alterations. Cholesterol biosynthesis is markedly inhibited by 25-OH. Triol has a lesser effect on cholesterol biosynthesis, but it is more potent in blocking uptake of cholesterol by arterial cells in culture. Cholesterol oxides may also influence cholesteryl ester accumulation by arterial smooth muscle cells. Incubation of cells with 25-OH resulted in a four-fold increase in cholesterol esterifying activity but no effect on cholesteryl ester hydrolytic activity. The cholesterol oxides appear to be transported in the blood primarily by very low density lipoproteins (VLDL) and low density lipoproteins (LDL). Oxidized LDL has cytotoxic effects and enhances macrophage lipid accumulation. These be effects may be directly related to the cholesterol oxide content of these lipoproteins.

Animals↗

Morphological changes in small vessels on endomyocardial biopsy.

Small vessel disease has been described in various cardiac conditions including diabetes mellitus, amyloidosis, and connective tissue disease. Less well understood is the incidence and morphological features of small vessel disease in patients with myocardial disease of unknown etiology. This study examines the incidence, clinical presentation, and pathological changes of small vessel disease in patients with normal epicardial coronary arteries undergoing endomyocardial biopsy. Biopsy specimens in 110 consecutive patients were analyzed by light and electron microscopy. Small vessel abnormalities were present in 16 patients (14.6 percent) of whom five patients had associated hypertension and 11 patients had idiopathic small vessel disease. There were six males and 10 females with a mean age of 53 (26 to 76) years. Clinical presentations were arrhythmias, heart failure, or chest pain. The left ventricular ejection fraction was reduced (less than 50 percent) in 12 of these 16 patients. The morphological features of small vessel disease included marked thickening of the arterial wall owing to subendothelial deposits of heterogeneous electron dense materials consisting of microfibrils, collagen and elastic fibers, cellular debris, and other amorphous substances. Subendothelial deposits comprised a mean 60 percent (40 to 76 percent) of the arterial wall thickness.

Adolescent↗

Kasabach-Merritt syndrome-associated kaposiform hemangioendothelioma successfully treated with cyclophosphamide, vincristine, and actinomycin D.

PURPOSE: The authors introduced a successful trial of a chemotherapy regimen to treat refractory thrombocytopenia and pain caused by a rare kaposiform hemangioendothelioma that had been refractory to corticosteroids. PATIENT AND METHOD: A 6-year-old Latina girl with diffuse petechiae, constant pain and edema in her right lower extremity, and severe thrombocytopenia was brought for treatment. Physical examination revealed a large mass in the right lower extremity. The surgical specimen resected earlier in Mexico showed kaposiform hemangioendothelioma, an extremely rare vascular tumor that is frequently associated with consumptive coagulopathy and lymphangiomatosis. Corticosteroid therapy in Mexico had been ineffective in controlling the tumor size, pain, or thrombocytopenia. The patient was brought to the United States because of a rapidly enlarging tumor and intractable leg pain, causing inability to ambulate. Laboratory examinations revealed profound thrombocytopenia and evidence of consumptive coagulopathy. Because of the rapidly enlarging lesion, it was decided to give six cycles of a chemotherapy regimen consisting of vincristine, cyclophosphamide, and actinomycin D (VAC). RESULT: The patient responded to the first cycle of chemotherapy with partial reversal of the thrombocytopenia. The additional five cycles of the same chemotherapy regimen resulted in complete resolution of thrombocytopenia and significant improvement of the pain and edema in the right lower extremity. A follow-up imaging study 9 months later revealed a marked decrease in size of the vascular tumor. CONCLUSION: Inoperable kaposiform hemangioendothelioma unresponsive to corticosteroids can be successfully treated with chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗