14 results on '"Sidawy, A.N."'
Search Results
2. Carotid Endarterectomy under General Anesthesia in ASA Class 3 or 4: A Safe Practice?
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Vettukattil, A., primary, Cryer, C., additional, Macsata, R., additional, and Sidawy, A.N., additional
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- 2009
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3. The effects of cilostazol on insulin-induced proliferation and migration of human diabetic infragenicular arterial smooth muscle cells
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Wakefield, M.C., primary, Kellicut, D.C., additional, Arora, S., additional, Weiswasser, J.M., additional, and Sidawy, A.N., additional
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- 2003
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4. Effect of Growth Factors on Cell Proliferation and Epithelialization in Human Skin
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Bhora, F.Y., primary, Dunkin, B.J., additional, Batzri, S., additional, Aly, H.M., additional, Bass, B.L., additional, Sidawy, A.N., additional, and Harmon, J.W., additional
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- 1995
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5. MEASUREMENT OF GLYCOGENIN UTILIZATION FOR GLYCOGEN SYNTHESIS IN TYPE II DIABETIC CELLS BY USE OF A SPECIFIC IMMUNOASSAY FOR APO-GLYCOGENIN
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Bailey, J.M., primary, Lillehoj, E.P., additional, Sidawy, A.N., additional, Jones, B., additional, and Cohen, J.L., additional
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- 1995
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6. Folic acid inhibits homocysteine-induced proliferation of human arterial smooth muscle cells
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Carmody, B.J., Arora, S., Avena, R., Cosby, K., and Sidawy, A.N.
- Abstract
Purpose: An elevated plasma homocysteine level has been identified as an independent risk factor for atherosclerosis. Whether this represents a marker for vascular disease or a direct effect on the vasculature remains unclear. Because vascular smooth muscle cells (VSMCs) play an integral role in the atherosclerotic process, we studied the effect of homocysteine on human infragenicular VSMC proliferation and the role of folic acid in reversing the homocysteine effect. Methods: Human infragenicular VSMCs harvested from amputation specimens were studied. Various cell groups were exposed to physiologic (6.25 @mmol/L and 12.5 @mmol/L) and pathologic (25 @mmol/L to 500 @mmol/L) concentrations of homocysteine. Similar groups were simultaneously exposed to 20 nmol/L of folic acid. Cell counts and DNA synthesis, as reflected by [methyl-^3H]-thymidine incorporation, were performed at 6 days and 24 hours, respectively. Additional groups were exposed to various combinations of folic acid (20 nmol/L), vitamin B"6 (145 nmol/L), and vitamin B"1"2 (0.45 nmol/L) in the presence of homocysteine (25, 50, and 250 @mmol/L). Results: Homocysteine resulted in a dose-dependent increase in DNA synthesis and cell proliferation. Cell counts increased significantly at homocysteine concentrations ranging from 25 @mmol/L to 500 @mmol/L (P < .05), with a maximal increase of 98% at 500 @mmol/L of homocysteine. The addition of 20 nmol/L folic acid resulted in significant inhibition of cell proliferation at all homocysteine concentrations studied (P < .001). Maximal inhibition of 70% occurred in the cells exposed to 50 @mmol/L of homocysteine. The increases in [methyl-^3H]-thymidine incorporation ranged from 36% at 6 @mmol/L homocysteine to a maximum of 247% at 500 @mmol/L homocysteine. All increases were statistically significant (P < .05). The addition of 20 nmol/L folic acid resulted in significant inhibition of DNA synthesis (P < .002). Vitamins B"6 and B"1"2 did not demonstrate significant antiproliferative properties. Conclusion: A possible role of homocysteine in the formation of atherosclerotic lesions is through a direct proliferative effect on VSMCs in a dose-dependent fashion. Folic acid intake at levels available in dietary supplements may prove protective in hyperhomocysteinemia-induced atherosclerosis. Vitamins B"6 and B"1"2 alone do not appear to exhibit a substantial inhibitory effect in the setting of elevated homocysteine levels. (J Vasc Surg 1999;30:1121-8.)
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- 1999
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7. Accelerated carotid artery disease after high-dose head and neck radiotherapy: Is there a role for routine carotid duplex surveillance?
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Carmody, B.J., Arora, S., Avena, R., Curry, K.M., Simpkins, J., Cosby, K., and Sidawy, A.N.
- Abstract
Purpose: High-dose external radiotherapy used in the treatment of head and neck carcinoma has been implicated as a risk factor for accelerated atherosclerotic disease of the carotid arteries. However, how radiotherapy affects atherosclerotic disease is controversial, and little data exist to demonstrate a strong relationship between radiotherapy and progressive carotid disease. Methods: We performed a retrospective chart review of 69 patients (all men) who underwent duplex ultrasound scanning examinations for carotid disease between 1993 and 1998. Twenty-three patients had received high-dose radiotherapy for the treatment of head and neck carcinoma within the past 12 years (group 1; mean age, 67.8 years), and 46 patients were randomly selected as age-matched control subjects (group 2; mean age, 68.3 years). The mean radiation dose was 6060 +/- 182 rads, and the average interval between radiotherapy and ultrasound scanning was 6.5 +/- 1.8 years. There was no significant difference between the two groups in the presence of these comorbidities: diabetes mellitus, coronary artery disease, hypertension, tobacco use, hypercholesterolemia, peripheral vascular disease, or stroke. Similarly, there was no difference in the indications for the duplex scanning studies. Results: Five of the 23 patients in group 1 (21.7%) were found to have advanced carotid disease (70% to 99% stenosis); four patients were symptomatic, three patients went on to endarterectomy, and one patient was awaiting surgery. Two of the 46 patients in the control group (4%) had advanced carotid disease. One patient was symptomatic, and both patients underwent endarterectomy. A significant difference in the prevalence of advanced disease between the two groups was noted (P = .037). Sixteen patients who survived irradiation underwent a second duplex scanning study and had evidence of progressive disease with significant increases in peak systolic velocities. Conclusion: High-dose radiotherapy to the head and neck region may be a significant risk factor for accelerated carotid atherosclerotic disease. Routine carotid duplex surveillance may be warranted in this high-risk patient population. (J Vasc Surg 1999;30:1045-51.)
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- 1999
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8. Transforming growth factor @b1 inhibits the proliferative effect of insulin on human infragenicular vascular smooth muscle cells
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Center, Veterans Affairs Medical, Washington, George, From the Departments of Surgery, Georgetown University Medical Centers., Forsyth, E.A., Aly, H.M., Najjar, S.F., Neville, R.F., and Sidawy, A.N.
- Abstract
Purpose: The distribution of atherosclerotic arterial disease in diabetes mellitus characteristically involves the infragenicular arterial tree including the anterior tibial, posterior tibial, and peroneal arteries. The proliferation of vascular smooth muscle cell (VSMC) is essential in the development of the atherosclerotic lesion. It has long been held that insulin plays a causative role in the formation of the atherosclerotic lesion in diabetes. We studied the role played by insulin in the proliferation of these cells in culture and the interaction of insulin with transforming growth factor beta 1 (TGF@b1), a factor known for its possible inhibitory effects. Methods: We have grown and characterized a line of VSMC harvested from atherosclerotic infragenicular arteries of human subjects undergoing below-knee amputation. The cultures were defined as being of VSMC origin by immunohistochemical staining with @a-smooth muscle actin. Confluent cultures of passages 4 through 7 were seeded into six well plates at a density of 5000 cells/well. After serum deprivation the cells were exposed to insulin (100 ng/ml) alone or in combination with TGF@b1 (6 ng/ml). Results: Our findings indicate that a 48-hour incubation with insulin augments the proliferation of human infragenicular VSMC, producing a 207% increase in cell number when compared with control cells (11,328 +/- 686, n = 56 vs 3682 +/- 182, n = 87; p < 0.0001). The addition of TGF@b1 in combination with insulin abolished the accelerated growth rate seen in test groups treated with insulin alone (3614 +/- 247, n = 32 vs 11,328 +/- 686, n = 56; p < 0.0001). Conclusion: These results strongly suggest that insulin is a potent stimulant of human infragenicular VSMC proliferation. The mitogenic effect of insulin is inhibited by TGF@b1, producing proliferation rates comparable to those observed in control cells incubated with serum-free media. (J Vasc Surg 1997;25:432-6.)
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- 1997
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9. Insulin-like growth factor-I binding in injury-induced intimal hyperplasia of rabbit aorta
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Sidawy, A.N., Hakim, F.S., Jones, B.A., Norberto, J.M., Neville, R.F., and Korman, L.Y.
- Abstract
Purpose: The proliferation of arterial-wall smooth muscle cells is an important step in the formation of intimal hyperplasia. Insulin-like growth factor-I (IGF-I) is a mitogen that exerts its effects through specific receptors located on the cell membrane. IGF-I has been found to promote the multiplication of vascular smooth muscle cells in culture. This study aimed to evaluate the status of IGF-I binding in injury-induced intimal hyperplasia in a rabbit model. Methods: We used binding techniques to study IGF-I binding of control and hyperplastic aortas of adult White New Zealand rabbits. Hyperplasia was induced by balloon-catheter injury. At 2 weeks and 1, 2, 4, and 7 months after injury, segments of abdominal aortas were harvested from two control and six study rabbits, and 20-@mm-thick frozen sections were obtained. Hematoxylin and eosin stained sections confirmed the presence of intimal hyperplasia in the hyperplastic aortas. Adjacent sections were incubated in a buffer solution containing ^1^2^5I-IGF-I in the presence and absence of an excess of unlabeled IGF-I. Autoradiograms were then obtained by apposing the treated sections to autoradiography film, which was developed at 3 days and analyzed by comparison with the hematoxylin and eosin stained sections under light microscopy. A marked increase in IGF-I binding grain density was observed in the areas corresponding to the hyperplastic lesions. To characterize these binding sites, binding inhibition studies were performed and the dissociation constant (K"d) and maximum binding capacity (B"m"a"x) were obtained from Scatchard analysis. Results: Six hyperplastic aortas for each time interval and a total of nine control aortas were evaluated. The K"d of the hyperplastic aortas (1.5 +/- 0.2 nmol/L) was not significantly different from that of control aortas (1.3 +/- 0.2 nmol/L), which indicated similar high-affinity IGF-I binding sites in normal and hyperplastic arteries. The results of B"m"a"x were 6.9 +/- 1.2, 8.5 +/- 2.1, 12.4 +/- 2.1, 20.4 +/- 5.9, 20.6 +/- 3.2, and 8.1 +/- 1.3 pmol/L for control, 2 weeks, 1 month, 2 months, 4 months, and 7 months, respectively. With analysis of variance (p < 0.05), B"m"a"x values at 1, 2, and 4 months were significantly higher than those of control aortas. B"m"a"x values returned to levels not significantly different from those of control aortas at the 7-month interval. Conclusion: Increased IGF-I binding in the hyperplastic aortas suggests that IGF-I plays an important role in the proliferation of arterial wall cellular components during the hyperplastic process. (J VASC SURG 1996;23:308-13.)
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- 1996
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10. The protective effect of vein cuffed anastomoses is not mechanical in origin
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Norberto, J.J., Sidawy, A.N., Trad, K.S., Jones, B.A., Neville, R.F., Najjar, S.F., Sidawy, M.K., and DePalma, R.G.
- Abstract
Purpose: Intimal hyperplasia (IH) is a proliferative process of vascular smooth muscle cells that occurs after an arterial injury, particularly at outflow anastomoses of prosthetic bypass grafts. IH causes stenosis that leads ultimately to graft flow reduction and thrombosis. We have demonstrated previously that vein cuff interposition between an expanded polytetrafluoroethylene (e-PTFE) graft and artery at distal anastomoses diminished IH formation in the arterial outflow as compared with noncuffed anastomoses. Improved long-term patency rates associated with the placement of an interposition vein cuff at the distal anastomosis of e-PTFE grafts to infrageniculate arteries have also been demonstrated clinically. This study examined the mechanical factors that may contribute to the protective effect of cuffed anastomoses. These factors include the expansibility of the vein cuff as compared with e-PTFE, as well as the angle of the cuffed anastomosis. Methods: Compatible animals were selected by use of platelet aggregation studies. Nine dogs, group A, received a 4 mm e-PTFE graft plus a 1 cm long interposition vein cuff at the distal anastomosis in the left carotid artery. The same procedure was done on the right side, and in addition the vein cuff was encircled by an e-PTFE jacket incorporated into the anastomosis to prevent the expansion of the vein cuff with arterial pulsation. To study the effect of distal anastomotic angle and geometry on the formation of IH, five dogs, group B, received a 4 mm e-PTFE graft in both sides. On the left, the distal anastomosis was performed between the graft and the artery at an acute angle as it is commonly done when a bypass graft is placed. On the right side a 1 cm long, 6 mm diameter e-PTFE segment was interposed between the artery and the graft at a perpendicular angle. This geometry mimicked the right angle of a vein cuff - to-artery anastomosis. After 10 weeks the grafts were harvested, and the thickness of IH was measured with an ocular micrometer under light microscopy. Results: In group A, one dog had bilateral graft thrombosis (12%), and these grafts were discarded. In the remaining eight dogs there was no statistically significant difference in the thickness of IH between the right (jacketed group) and the left side (nonjacketed/control group), showing that vein cuff expansibility did not play a role in protecting against the formation of IH. In group B, bilateral graft thrombosis occurred in four of five dogs (80%), suggesting that the perpendicular anastomotic angle was not protective. Conclusion: These results suggested that the protective effect of the vein cuff is not mechanical in origin. (J VASC SURG 1995;21:558-66.)
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- 1995
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11. Proliferation and extracellular matrix production by human infragenicular smooth muscle cells in response to interleukin-1@b
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Forsyth, E.A., Aly, H.M., Neville, R.F., and Sidawy, A.N.
- Abstract
Purpose: Atherosclerotic peripheral vascular disease commonly involves the infragenicular arterial tree. Our study evaluated the effect of interleukin (IL)-1@b on the proliferation of vascular smooth muscle cells (VSMCs) derived from atherosclerotic infragenicular arteries of human subjects who underwent below-knee amputation, as well as the role of IL-1@b in VSMCs' production of extracellular matrix components, substances that are important in the transformation of VSMCs from the contractile to the synthetic phenotype. This transformation to the synthetic phenotype is an important step in the formation of the atherosclerotic lesion. Methods: Cultures were identified as being of smooth muscle origin through staining with the cytoskeletal marker, @a-smooth muscle actin. Proliferation assays were performed by seeding confluent cultures of passages 4 to 7 into six-well plates at 10,000 cells per well. After serum starvation, samples were incubated with IL-1@b (1 ng/ml). Cell number was determined on a daily basis. To study extracellular matrix production, cells were propagated in tissue culture chamber slides in the absence or presence of growth media containing IL-1@b. After fixation with 100% methanol, each sample was stained with a primary antibody specific for an extracellular matrix component. After staining with the fluorescein-tagged secondary antibody, each sample was examined using immunofluorescent microscopic examination. Results: The results of our proliferation assays showed that IL-1@b caused a significant increase in the proliferation of VSMCs at 24, 48, 72, and 96 hours (p H 0.003 when comparing IL-1@b-treated samples with control specimens at each time period using unpaired t test). The number of IL-1@b-treated cells at 96 hours was double the number present in the control samples (16,033 +/- 238 vs 8102 +/- 824). When compared with control samples, IL-1@b was found to affect the production of extracellular matrix proteins by infragenicular VSMCs. IL-1@b caused an increase in the production of fibronectin, a decrease in the production of laminin, and no change in the production of collagen type IV. Conclusions: These results suggest that interleukin-1@b acts as a potent stimulant of the proliferation of human infragenicular VSMCs. IL-1@b also acts to augment the production of fibronectin by these cells. Fibronectin has been implicated in the phenotypic transformation of VSMCs from the contractile to the synthetic state. Therefore, IL-1@b may serve as an important regulatory factor in the development of atherosclerosis by stimulating the proliferation of VSMCs and their transformation to the synthetic state, two important steps in the formation of the atherosclerotic lesion. (J Vasc Surg 1997;26:1002-8.)
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- 1997
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12. Insulin-like growth factor-1receptors mediate infragenicular vascular smooth muscle cell proliferation in response to glucose and insulin not by insulin receptors - effects on smooth muscle cell proliferation
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Avena, R., Mitchell, M.E., Carmody, B., Arora, S., Neville, R.F., and Sidawy, A.N.
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- 1999
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13. Phenotypic characterization of human smooth muscle cells derived from atherosclerotic tibial and peroneal arteries
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Jones, B.A., Aly, H.M., Forsyth, E.A., and Sidawy, A.N.
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Purpose: The vascular smooth muscle cell plays a pivotal role in the development of atherosclerosis. The objectives of this study were to characterize smooth muscle cells from the human atherosclerotic tibial artery to determine their phenotypic properties and to examine the contractile reactions of these cells to physiologic and pharmacologic stimuli. Methods: After below-knee amputations were performed, vascular smooth muscle cells were harvested and cultivated from tibioperoneal source. Characterization was done with transmission electron microscopy and immunocytochemistry. The contractile properties were determined by observing the response to various stimuli. In addition, segments of vessels harvested were submitted to electron microscopy studies for comparison with the cultured cells. Results: Immunofluorescent labeling was positive for @a-smooth muscle actin. Electron microscopy revealed the presence of a thickened basal laminae and large intracellular lipid vacuoles. The earlier passages revealed cells with a large number of microfilaments characteristic of a contractile cell. As later passages were examined, there was a notable change in character with an increasing amount of rough endoplasmic reticulum and Golgi complexes. The increased thickness of the basal lamina in the cultured cells resembled that found in vessel segments studied by electron microscopy. A rapid contraction response was seen when the cells were incubated with angiotensin II, bradykinin, or endothelin. No response was seen with the addition of isoproterenol, nitroglycerin, or nitroprusside, known smooth-muscle relaxants. Conclusion: This model demonstrates the apparent inability of these smooth muscle cells from atherosclerotic tibial arteries to relax to pharmacologic and physiologic stimuli. In addition, as seen by transmission electron microscopy, these cells maintain their atherosclerotic phenotype after multiple passages. (J Vasc Surg 1996;24:883-91.)
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- 1996
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14. The effect of occult diabetic status and oral glucose intake on brachial artery vasoactivity in patients with peripheral vascular disease
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Avena, R, Curry, K.M, Sidawy, A.N, Simpkins, J.F, Neville, R.F, Mitchell, M.E, and Bukowski, M
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- 1998
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