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Biomedical subjects

Y S Do

Publications and source records attributed to Y S Do.

At least 37 records · Page 2Linked to original sources
PubMed1999

Regenerative nodules in liver cirrhosis: findings at CT during arterial portography and CT hepatic arteriography with histopathologic correlation.

PURPOSE: To determine the appearance of regenerative nodules in patients with liver cirrhosis at computed tomography (CT) during arterial portography (CTAP) and CT hepatic arteriography (CTHA). MATERIALS AND METHODS: CTAP and CTHA of the liver were performed in 28 consecutive patients with hepatocellular carcinoma (HCC) who were scheduled to undergo partial resection of the liver. Helical CTAP was performed after contrast material injection into the superior mesenteric artery followed by helical CTHA after contrast material injection into the hepatic artery. CT scans were analyzed for the presence of identifiable nodules and their size; results were correlated with gross and microscopic findings. RESULTS: Resected livers showed cirrhosis in 20 patients, chronic hepatitis in four, and normal liver in four. Among the 20 patients with cirrhosis, regenerative nodules were demonstrated as enhancing 3-10 mm nodules surrounded by lower attenuation fibrous septa 0.8-1.5 mm thick at CTAP in seven patients and nonenhancing nodules of the same size surrounded by enhancing fibrous septa at CTHA in 15 patients. The degree of fibrosis determined the conspicuity of nodules. CONCLUSION: Regenerative nodules in cirrhotic liver are visualized as enhancing nodules surrounded by lower attenuation thin septa at CTAP and nonenhancing nodules surrounded by enhancing fibrous septa at CTHA. CTHA is more sensitive than CTAP in depicting regenerative nodules (P < .005).

Carcinoma, Hepatocellular↗
PubMed1999

Upper gastrointestinal tract malignant obstruction: initial results of palliation with a flexible covered stent.

The authors treated 21 patients with inoperable upper gastrointestinal tract malignant obstruction from the esophagus to the duodenum by means of intubation with a flexible covered stent with fluoroscopic guidance. Stent placement was successful and relief of dysphagia was immediate in 18 (86%) patients, without serious complication. The average dysphagia score decreased from 2.6 (dysphagia to liquids) to 1.0 (dysphagia to normal solid food). Placement of a flexible covered stent provides easy, safe, and effective palliation of upper gastrointestinal malignant obstruction.

Adult↗
PubMed1999

Splanchnic arterial stenosis or occlusion: diagnosis at Doppler US.

PURPOSE: To determine the diagnostic accuracy of Doppler ultrasonography (US) in the detection of high-grade stenosis or occlusion of the celiac artery (CA) and superior mesenteric artery (SMA) and validate the previously reported Doppler US criteria. MATERIALS AND METHODS: During a recent 36-month period, 82 patients were prospectively examined with Doppler US of the splanchnic arteries and with lateral abdominal aortography, regardless of their abdominal symptoms. The previously reported diagnostic criteria with the fasting peak systolic velocity measurement were prospectively used in all patients. The results of Doppler US were compared with those of lateral aortography. RESULTS: The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of Doppler US for the detection of 70% or greater CA stenosis or occlusion were 100%, 87%, 57%, 100%, and 89%, respectively; for 70% or greater SMA stenosis or occlusion, these values were 100%, 98%, 93%, 100%, and 99%, respectively. CONCLUSION: Owing to its high accuracy in the diagnosis of high-grade splanchnic arterial stenosis or occlusion, Doppler US can be used as a screening method to help detect CA or SMA stenosis or occlusion and can reduce the use of unnecessary, invasive angiography.

Aged↗
PubMed1998

Malignant colorectal obstruction: treatment with a flexible covered stent.

PURPOSE: To evaluate the usefulness of flexible covered stents for treatment of acute colorectal obstruction secondary to malignant colorectal carcinoma. MATERIALS AND METHODS: Twenty patients with acute colorectal obstruction secondary to malignant colorectal carcinoma were treated by means of intubation of a flexible stent with fluoroscopic guidance with occasional endoscopic assistance. Two types of stents were placed (type 1, completely covered, type 2, two-thirds of proximal part uncovered). Of 15 patients with primary colorectal carcinoma, 12 underwent placement of a stent for presurgical decompression of colorectal obstruction; three, for palliative decompression. In three patients with rectosigmoid seeding from advanced gastric carcinoma and two patients with recurrent colonic carcinoma, stents were placed for palliative decompression. RESULTS: Stent placement was successful in 18 (90%) of 20 patients. Symptoms of obstruction resolved within 24 hours in 15 (75%) patients. Eight patients underwent elective single-stage surgery without complications 5-7 days after stent placement. Two patients underwent tumor resection and colostomy. In eight patients, stents provided palliative decompression of the colon. Type 1 stents migrated in four (50%) of eight patients; type 2 stents were used thereafter. CONCLUSION: Flexible stents effectively relieved acute colonic obstruction secondary to malignant rectosigmoid neoplasm. Stent placement allowed patients to undergo single-stage surgery in most cases and provided palliative decompression in cases of inoperable or disseminated disease.

Acute Disease↗
PubMed1998

Integrins, adhesion, and cardiac remodeling.

Integrins are heterodimeric cell surface receptors that mediate a cell's ability to perceive its environment, respond to changed in its environment, and alter its environment. When activated, these receptors form focal adhesions, which are areas of close attachment of the cells to extracellular matrix proteins in which colocalization of cytoskeletal proteins, intracellular signaling molecules, and growth factor receptors occurs. In cardiac fibroblasts, integrins mediate cell growth and adhesion. Growth factors such as angiotensin II regulate DNA synthesis, protooncogene expression, extracellular matrix production, adhesion, and other actions of cardiac fibroblasts, many of which require integrin activation. In addition to controlling growth factor and hemodynamic effects, regulation ofintegrin activity may be useful to affect cardiac fibrosis and the remodeling process.

Animals↗
PubMed1997

Myocardial osteopontin expression is associated with left ventricular hypertrophy.

BACKGROUND: Osteopontin (OP) has been identified in cultured rat cardiac fibroblasts, where it contributes to angiotensin II (AII)-induced remodeling processes; in cultured cardiomyocytes; and in macrophages in cardiac tissues with inflammation. However, the presence of OP has not been reported in histological sections of myocardial tissue. In the present study, we investigated (1) the regulation of OP mRNA expression in cultured rat cardiomyocytes; (2) the localization of OP mRNA in neonatal and adult normal and hypertrophied rat hearts; and (3) the histology of OP expression in myocardial specimens from humans either with myocyte hypertrophy or with no pathological changes. METHODS AND RESULTS: Cultured neonatal cardiomyocytes expressed OP mRNA and were immunoreactive for OP. Endothelin-1 (ET-1) and norepinephrine (NE) increased both OP and atrial natriuretic peptide (ANP) mRNA levels twofold to threefold (P<.01). OP mRNA was prominent in ventricular tissue from neonatal and adult rats with renovascular hypertension and aortic banding, whereas barely detectable levels were observed in normal adult cardiac tissue. ANP and OP mRNA levels in normal and hypertrophied ventricles correlated (r2=.87, P<.001). OP immunoreactivity and mRNA transcripts were predominantly found in cardiomyocytes not associated with inflammatory cells in sections from neonatal and adult hypertrophied hearts. No staining was detectable in normal adult hearts. Human myocardium with extensive fibrosis and cardiomyocyte hypertrophy obtained from explanted hearts with either idiopathic (n=5) or ischemic cardiomyopathy (n=7) demonstrated substantial myocyte immunoreactivity for both OP and ANP in right and left ventricles that was not associated with leukocyte infiltration. In situ hybridization identified cardiomyocytes as the major source of OP mRNA transcripts in these hearts. In contrast, OP immunoreactivity was not detectable in four of five endomyocardial biopsies with normal histology. CONCLUSIONS: The present study provides the first evidence that cardiomyocytes are a prominent source of OP in vivo and suggests that induction of OP expression is strongly associated with ventricular hypertrophy.

Animals↗
PubMed1997

Expandable metallic stent placement in patients with benign esophageal strictures: results of long-term follow-up.

PURPOSE: To evaluate the long-term effectiveness of expandable esophageal metallic stents in benign esophageal strictures. MATERIALS AND METHODS: The authors performed long-term follow-up of 14 expandable metallic stents in 12 patients (aged 16-72 years) with benign esophageal strictures. All 12 patients had initially undergone placement of one stent; two patients received an additional stent because of recurrent dysphagia. RESULTS: No procedural complications occurred. Delayed complications occurred in all patients. New strictures formed in six stents (five patients), migration occurred in seven stents (six patients), and both migration and formation of new strictures occurred in one stent (one patient). New stricture formation caused recurrence of dysphagia and necessitated further treatment. Three of four stents that migrated within 2 months after placement but none of the four stents that migrated more than 2 months after placement caused recurrence of dysphagia. Six patients died of unrelated causes 6-20 months after stent placement. The remaining six patients are still alive 24-48 (mean, 35) months after stent placement. CONCLUSION: The long-term effectiveness of expandable metallic stents in benign esophageal strictures is not encouraging because of the high delayed-complication rate. That the patients with migration showed improvement of dysphagia, however, may warrant further investigation of temporary placement of a retrievable covered stent.

Adolescent↗
PubMed1997

Angiotensin II promotes remodelling-related events in cardiac fibroblasts.

Remodelling is a fundamental cardiac response to injury, and involves cardiac fibroblast proliferation and extracellular matrix production. Angiotensin II (A II) directly promotes these changes in cardiac fibroblasts, and is thus a critical element in cardiac hypertrophy and a processor of wound healing. Osteopontin mRNA was readily detectable in total RNA harvested from cultured neonatal and adult cardiac fibroblasts. Immunocytochemical staining of cultured adult cardiac fibroblasts grown on coverslips revealed the presence of beta 3 integrin on the surfaces of the cells. In the present study, we investigated the role of A II in a model of wound healing using floating collagen gels harboring adult rat cardiac fibroblasts. The presence of a monoclonal antibody against osteopontin, MPIIIB10, at 7.2 micrograms/ml, or the arginine-glycine-aspartate (RGD) peptide (10(-4) M), had no effect on gel contraction. Osteopontin itself induced fibroblast gel contraction (79.1 +/- 3.8%). But this effect of osteopontin was completely neutralized by MPIIIB10 (7.2 micrograms/ml), RGD peptide (10(-4) M), and monoclonal antibody against rat beta 3 integrin (25 micrograms/ml). These results suggest that A II promotes cardiac wound healing and remodelling processes by inducing osteopontin and beta 3 integrin in cardiac fibroblasts.

Angiotensin II↗
PubMed1996

Osteopontin is produced by rat cardiac fibroblasts and mediates A(II)-induced DNA synthesis and collagen gel contraction.

Angiotensin II (AII) is a critical factor in cardiac remodeling which involves hypertrophy, fibroblast proliferation, and extracellular matrix production. However, little is known about the mechanism by which AII accelerates these responses. Osteopontin is an acidic phosphoprotein with RGD (arginine-glycine-aspartate) sequences that are involved in the vascular smooth muscle cell remodeling process. We identified the presence of osteopontin mRNA and protein in cultured rat cardiac fibroblasts and its prominent regulation by AII (10(-11) M). Osteopontin message levels were increased fourfold (P < 0.01) and protein fivefold (P < 0.05) at 24 h after addition of AII (10(-7) M). This response was inhibited by the AT1 receptor blocker, losartan. Osteopontin mRNA levels were increased in hypertrophied ventricles from animals with renovascular hypertension (1.6-fold, P < 0.05) and aortic banding (2.9-fold, P < 0.05). To examine the function of osteopontin, we determined its effects on (a) the ability of cardiac fibroblasts to contract three-dimensional collagen gels and (b) cardiac fibroblast growth. A monoclonal antibody against osteopontin partially blocked AII-induced three-dimensional collagen gel contraction by cardiac fibroblasts (64+/-4 vs. 86+/-5% in the presence of antibody, P < 0.05), while osteopontin itself promoted contraction of the gels by fibroblasts (71+/-5%, P < 0.05 compared with control). Either a monoclonal antibody against beta3 integrin which is a ligand for osteopontin or the RGD peptide blocked both AII and osteopontin-induced collagen gel contraction. Thus, the osteopontin RGD sequence binds to beta3 integrins on the fibroblast to promote fibroblast binding to collagen. All induced a threefold increase in DNA synthesis of cardiac fibroblasts, which was completely blocked by antibodies against osteopontin and beta3 integrin, or by RGD peptide, but not by controls. Thus, All-induced growth of cardiac fibroblasts also requires osteopontin engagement of the beta3 integrin. Taken together, these results provide the first evidence that osteopontin is a potentially important mediator of AII regulation of cardiac fibroblast behavior in the cardiac remodeling process.

Angiotensin II↗
PubMed1996

Comparison of ANG II with other growth factors on Egr-1 and matrix gene expression in cardiac fibroblasts.

The purpose of the present investigation was to compare the effects of angiotensin II (ANG II) other growth factors implicated to play a role in ventricular hypertrophy on cardiac fibroblast changes associated with cardiac remodeling. These changes included induction of early growth response (Egr-1) gene and increases in message levels of extracellular matrix proteins. ANG II treatment (10(-10)-10(-6) M) of rat cardiac fibroblasts induced 1) Egr-1 and 2) a fourfold (P < 0.02) increase in fibronectin and a twofold (P = 0.05) increase in laminin mRNA levels but no increases in that of collagens I, III, or IV at 24-48 h, and 3) a decrease in AT1-receptor mRNA levels to 26% (P < 0.001) of basal at 4-6 h. These effects were all inhibited by the AT1-receptor blocker, losartan, but not AT2-receptor blockers. Immunostaining of cultured cells with antibody against rat fibronectin demonstrated positive staining of cells in serum-free medium; staining was more intense in cells treated with ANG II (10(-6) M, 48 h). Fluorescent-activated cell sorting using an antibody against rat AT1 receptor demonstrated a receptor signal in cells maintained in serum-free medium; however, the receptor signal was not detectable in ANG II-treated cells. Serum and epidermal growth factor (EGF) also induced Egr-1, but norepinephrine (NE) and endothelin (ET) had no effect. Serum increased fibronectin mRNA levels by twofold (P < 0.05). EGF, NE, and ET had no effect on matrix gene expression. Serum, EGF, and NE also transiently downregulated AT1-receptor mRNA levels at 4-6 h of treatment. These results demonstrate that 1) ANG II both induces protooncogene expression and enhances fibronectin mRNA levels in cultured cardiac fibroblasts, whereas EGF only induces Egr-1, and NE and ET have no effects on either function; 2) ANG II effects are primarily mediated by the AT1 receptor; and 3) growth factors can regulate AT1-receptor mRNA levels. Thus ANG II, relative to NE, ET, and EGF, appears to play a prominent and direct role in fibroblast changes associated with cardiac hypertrophy.

Angiotensin I↗
PubMed1995

Angiotensin II in cell growth and matrix production.

Glomerular mesangial cells and cardiac fibroblasts have been called "myofibroblasts" because of their phenotypic characteristics (resembling both the fibroblast and muscle cells). Thus, it is not surprising that AII would have similar effects on both cell types, which play critical roles in target organ stress response and wound healing, ultimately leading to remodeling changes. These effects are primarily mediated by the AT1 receptor and include: 1) growth: hyperplasia in cardiac fibroblasts and hypertrophy in normal adult mesangial cells and 2) matrix production: there appears to be an early upregulation of fibronectin message which is later followed by an increase in collagens. It is likely that elevated production of fibronectin may activate signal transduction pathways which lead to increased expression of collagen genes, and which may be critical for the organization and laying down of collagens. Thus, an overall theme that emerges is the impact of AII on both growth and wound repair. Other potential important cellular effects of AII in these systems include: 1) stimulation of growth factors, cytokines, and arachidonic acid products that could have autocrine or paracrine effects, 2) regulation of cell migration and adhesion, 3) alteration of responses to neurohormones, 4) development and maintenance of a differentiated phenotype, and others. Molecular techniques including subtraction hybridization, differential display, antisense knockout, and development of transgenic and embryonic stem cell models will be important in defining the specific role of AII in cardiovascular and renal disease.

Angiotensin II↗
PubMed1995

Thoracic manifestations of Behçet syndrome: radiographic and CT findings in nine patients.

PURPOSE: To evaluate the radiographic and computed tomographic (CT) findings of patients with thoracic Behçet syndrome. MATERIALS AND METHODS: Chest radiographs and CT scans of nine patients with thoracic Behçet syndrome were retrospectively reviewed. Findings were compared. RESULTS: Radiographs of the nine patients showed mediastinal widening in five (56%), air-space consolidation in five (56%), and lung mass in three (33%). CT scans of the nine patients showed that mediastinal widening was due to thrombosis in four (44%) or narrowing of the superior vena cava in one [11%], which caused mediastinal edema; that air-space consolidation (seen on both radiographs and CT scans) was due to pulmonary hemorrhage or infarction in five (56%); and that lung mass was due to aneurysm of the right or left pulmonary artery in three (33%). In addition, CT scans showed hyperinflation in one patient. CONCLUSION: Chest radiographic findings of thoracic Behçet syndrome are variable and nonspecific. CT can be helpful in the assessment of the syndrome by showing thrombosis of the superior vena cava and characteristic aneurysms of the pulmonary arteries.

Adolescent↗
PubMed1994

Proximal 2.6 kb of 5'-flanking DNA is insufficient for human renin promoter activity in renin-synthesizing chorio-decidual cells.

In order to determine the influence of proximal 5'-flanking DNA of the human renin gene (REN) in cells that express human renin, transient expression analyses were carried out in chorio-decidual cells. Constructs containing different lengths of REN promoter DNA, extending as far as 2595 bp upstream of the transcription start site, were unable to drive transcription of a chloramphenicol acetyl transferase reporter gene in chorio-decidual cells, nor in noncognate 293 or JEG-3 cells. The tk promoter was similarly inactive in constructs containing -2595 to -453 fragments of REN 5'-flanking DNA. In each cell type, the -2595 to -1300 DNA exerted a negative influence. Additional promoter- and cell type-dependent negative influences were noted for other regions of REN 5'-flanking DNA and the -453 to -145 DNA increased tk promoter activity 2.5-fold in chorio-decidual cells. By introducing the SV40 enhancer into constructs, a weak stimulation of the REN promoter was observed in chorio-decidual cells, but not in noncognate, JEG-3 cells, although the -2595 to -1300 DNA retained its negative influence in the cognate cell type. These results show that the proximal 2.6 kb of REN 5'-flanking DNA is unable to drive reporter gene activity in renin-synthesizing, chorio-decidual cells under basal conditions and suggest that trans-acting factors unique to at least this cell type, together with enhancer(s) located outside of the proximal 2.6 kb of REN promoter DNA tested, could be required for human renin promoter activity.

Chorion↗
PubMed1994

Identification of cyclic AMP response element in the human renin gene.

In order to identify the mechanism by which cyclic AMP stimulates expression of the human renin gene (REN), the effect of forskolin was tested in transient expression analyses of REN 5'-flanking DNA-chloramphenicol acetyltransferase (CAT) reporter gene constructs in secondary cultures of human chorio-decidual cells, a major site of renin synthesis. Forskolin induced a mean 5-fold stimulation which was localized to DNA in the region -249 to -162 with respect to the transcription start site (+1). Such DNA also mediated a response to forskolin in heterologous (HSV thymidine kinase) promoter constructs. Strong cAMP-response element (CRE) homology at -222 to -218 resembled the target for members of the CRE binding protein (CREB) family. Gel shift assays demonstrated similarly migrating nucleoprotein complexes for oligonucleotides containing the putative REN CRE as for a canonical CRE, in chorio-decidual, JEG-3 and HeLa nuclear extracts. Mutation of residues critical for CREB attachment reduced binding. In conclusion, a CRE was identified at -222 to -218 that appears critical for cAMP-induced human renin gene transcription.

Animals↗
PubMed1994

Angiotensin II (AII) modulation of steroidogenesis by luteinized granulosa cells in vitro.

PURPOSE: The purpose of the present study was to evaluate the effect of angiotensin II and its inhibitor, saralasin, on steroid production by luteinized human granulosa cells in vitro. Granulosa cells were obtained from follicular fluid aspirations from human in vitro fertilization. Cultures were established in supplemented Ham's F-10 medium. Human chorionic gonadotropin and angiotensin II were added to culture media and the effect on steroid production was measured. RESULTS: Human chorionic gonadotropin alone stimulated production of progesterone, estradiol, and testosterone. The addition of angiotensin II resulted in a dose-dependent increase in progesterone production (428% increase compared to baseline). No effect was seen on estradiol or testosterone. However, a large increase (700%) in estradiol was seen with the addition of the competitive inhibitor of angiotensin II, saralasin. CONCLUSION: We conclude that angiotensin II modulates progesterone production by human luteinized granulosa cells in vitro. The observed enhancement of estradiol production by angiotensin blockade suggests a tonic inhibition of estradiol secretion by endogenous angiotensin II.

Angiotensin II↗
PubMed1994

Function of human renin proximal promoter DNA.

An understanding of the mechanisms involved in the control of the human renin promoter have been hampered and confounded in work to date because of deficiencies in material available and experimental design. The promoter appears to be weak and a good cell model is lacking. Chorio-decidual cultures have been used since these have high renin synthesis, are readily available and grow well in culture. They suffer, however, from phenotypic variability and do not transfect well in transient expression analyses. Recent evidence suggests that 2.6 kb of proximal 5'-flanking DNA is unable to induce native promoter activity under basal conditions. Experiments in which an exogenous enhancer was introduced have raised the possibility that an endogenous enhancer residing outside of the 2.6 kb 5'-flanking region could be required. Cell-type specific factors also appear to be needed. The proximal flanking DNA does, however, appear to be capable of conferring activity on the promoter in chorio-decidual cells under stimulated conditions, suggesting that factors so activated may have considerable importance. Evidence suggests that forskolin-responsive signal transduction pathways may lead cyclic AMP responsive element (CRE) binding protein (CREB) to act on a CRE at -222 in the proximal REN promoter DNA. Activation of the mouse promoter by cAMP appears to involve a different element, however. Furthermore, overall control of renin synthesis is likely to involve post-transcriptional mechanisms as well. Thus, despite being the first cardiovascular gene to be cloned, much more work is required before the control of the human renin gene is fully understood.

Animals↗