PubMed Health⌕ Search

Biomedical subjects

R Foti

Publications and source records attributed to R Foti.

At least 19 recordsLinked to original sources
PubMed2001

Long-term angiographic follow-up after successful repeat balloon angioplasty for in-stent restenosis.

BACKGROUND: Coronary stent implantation is associated with improved angiographic short-term and mid-term clinical outcome. However, restenosis rate still remains between 20 and 30%. HYPOTHESIS: The purpose of the study, performed as a prospective angiographic follow-up to detect restenosis, was to evaluate the immediate and the 6-month angiographic results of repeat balloon angioplasty for in-stent restenosis. METHODS: From April 1996 to September 1997, 335 stenting procedures performed in 327 patients underwent prospectively 6-month control angiography. Of the 96 lesions that showed in-stent restenosis (> 50% diameter stenosis) (29%), 72 underwent balloon angioplasty. RESULTS: The primary success rate was 100%. Follow-up angiogram at a mean of 6.9 +/- 2.4 months was obtained in 54 patients. Recurrent restenosis was observed in 24 of the 55 stents (44%). Repeat intervention for diffuse and body location in-stent restenosis before repeat intervention was associated with significantly higher rates of recurrent restenosis (p < 0.001 and p < 0.05, respectively). Of the 19 patients who underwent further balloon angioplasty (100% success rate), coronary angiography was performed in 18 (95%) at a mean of 8.2 +/- 2.0 months and showed recurrent restenosis in 12 patients (67%). Further repeat intervention for diffuse and severe in-stent restenosis before the second repeat intervention was associated with significantly higher rates of further recurrent restenosis (p < 0.05 and p < 0.005, respectively). CONCLUSIONS: Although balloon angioplasty can be safely, successfully, and repeatedly performed after stent restenosis, it carries a progressively high recurrence of angiographic restenosis rate during repeat 6-month follow-ups. The subgroup of patients with diffuse, severe, and/or body location in-stent restenosis proved to be at higher risk of recurrent restenosis.

Aged↗
PubMed2001

Tubules are the major site of M-CSF production in experimental kidney disease: correlation with local macrophage proliferation.

BACKGROUND: Local proliferation of macrophages occurs within both the glomerulus and the interstitium in severe forms of human and experimental glomerulonephritis and plays an important role in amplifying renal injury. Macrophage colony-stimulating factor (M-CSF) is thought to be the growth factor driving this local macrophage proliferation. Previous studies have found that glomeruli are the predominant source of M-CSF production. However, this is difficult to reconcile with the prominent macrophage accumulation and proliferation seen in the interstitial compartment in glomerulonephritis. To address this issue, we localized M-CSF expression in rat models of glomerular versus tubulointerstitial injury and examined its relationship to local macrophage proliferation. METHODS: M-CSF expression (Northern blotting, in situ hybridization, immunostaining, Western blotting) and local macrophage proliferation (double immunostaining) was examined in normal rat kidney on days 1 and 14 of rat anti-glomerular basement membrane (anti-GBM) glomerulonephritis and on day 5 following unilateral ureteric obstruction. RESULTS: M-CSF mRNA and protein expression were identified in small numbers of glomerular podocytes, approximately 25% of cortical tubules, and most medullary tubules in normal rat kidney. Northern blotting showed a significant increase in whole kidney M-CSF mRNA in rat anti-GBM glomerulonephritis. Up-regulation of glomerular and, most prominently, tubular M-CSF production was confirmed by three independent methods: in situ hybridization, immunostaining, and Western blotting. The increase in M-CSF expression colocalized with local macrophage proliferation (ED1+PCNA+ cells) in both the glomerulus and tubulointerstitium. On day 5 after ureter ligation, there was a significant increase in tubular M-CSF mRNA and protein expression in the obstructed kidney, with no change in glomerular M-CSF. In parallel with M-CSF expression, macrophage accumulation and proliferation was prominent in the interstitium, but was absent from glomeruli. CONCLUSIONS: The tubular epithelial cell is the major site of M-CSF production within the injured kidney. Indeed, substantial macrophage accumulation and local proliferation can occur in the tubulointerstitium in the absence of glomerular inflammation. These results suggest that M-CSF production within the kidney, particularly by tubular epithelial cells, plays an important role in regulating local macrophage proliferation in experimental kidney disease.

Animals↗
PubMed2001

[Aneurysms of the common trunk, anterior descending and right coronary artery in a 33 years old man with acute myocardial infarction. A case report].

Coronary artery aneurysms are often incidental findings during coronary angiography; they are mostly secondary to atherosclerosis or vasculitis, they are rarely congenital. Right coronary circumflex and anterior descending arteries are usually involved but only few cases of aneurysms of left main coronary artery are reported. A case of coronary artery aneurysms is described involving left main, right and anterior descending coronary arteries, probably secondary to atypical Kawasaki disease in a 33 years old man with acute myocardial infarction.

Adult↗
PubMed2000

Up-regulation of the tumour-associated marker CD44V6 in experimental kidney disease.

CD44 is an adhesion molecule involved in a wide range of cell-cell and cell-matrix interactions. The standard form of CD44 (CD44S) is a 85-90-kD glycoprotein, but alternative splicing of RNA encoding 10 variable exons (V1-V10) can give rise to many different CD44 variant protein isoforms of higher molecular weight. CD44 isoforms containing the V6 exon play a crucial role in tumour metastasis and lymphocyte activation. However, the role of CD44V6 in the kidney is unknown. The aim of this study was to examined renal CD44V6 expression in health, disease and in vitro. Immunohistochemistry staining with the V6-specific 1.1ASML antibody identified constitutive CD44V6 expression by occasional cortical tubular epithelial cells and medullary tubules in normal rat kidney. In immune-induced kidney disease (rat anti-glomerular basement membrane glomerulonephritis), there was a marked increase in CD44V6 expression by cortical tubules, particularly in areas of tubulointerstitial damage, which was associated with focal macrophage infiltration. There was also a marked increase in CD44V6 expression by damaged tubules in a model of non-immune kidney disease (unilateral ureteric obstruction). Reverse transcription-polymerase chain reaction revealed a complex pattern of CD44V6-containing mRNA isoforms in normal rat kidney. This pattern of CD44V6 splicing was essentially unaltered in disease. The NRK52E normal rat kidney tubular epithelial cell line expresses both CD44S and CD44V6. Stimulation of NRK52E cells with IL-1 or transforming growth factor-beta 1 induced a two-to-five-fold increase in the expression of both CD44S and CD44V6. Furthermore, triggering of NRK52E cells by antibodies to CD44S or CD44V6, but not isotype control antibodies, induced secretion of monocyte chemoattractant protein-1. In conclusion, this study has identified expression of the tumour-associated marker CD44V6 in tubular epithelial cells in normal and diseased rat kidney, and suggests that signalling through the CD44V6 molecule may participate in the pathogenesis of experimental kidney disease.

Animals↗
PubMed1999

Usefulness of platelet glycoprotein IIb/IIIa inhibitors in coronary stenting for reconstruction of complex lesions: procedural and 30 day outcome.

BACKGROUND: Intracoronary stent implantation during percutaneous transluminal coronary angioplasty (PTCA) has shown favorable results, reducing acute complications associated with PTCA, such as coronary artery dissection and abrupt or threatened vessel closure. However, treatment of lesions with a complex morphology and diffuse disease, requiring long or multiple coronary stents, is still associated with a poorer outcome. We investigated the hypothesis that abciximab might lead to a different outcome in patients with complex coronary lesions, which require long or multiple stent implantation. METHODS: One hundred and six patients were randomized to receive either a combination of abciximab (bolus and 12 hour infusion) and weight-adjusted low-dose heparin or weight-adjusted heparin alone and followed up to 30 days. RESULTS: The procedural success rate was 100% in both groups of patients. In the control group a composite rate of major adverse events such as any death irrespective of cause, Q wave or non-Q wave myocardial infarction, acute or subacute stent thrombosis and urgent revascularization of 15.3% was shown at 30-day follow-up. The use of abciximab reduced the composite adverse event rate to 3.7% (76% absolute reduction, p < 0.05). CONCLUSIONS: The use of abciximab during high risk stenting is safe and reduces the risk of cardiac events at 30-day follow-up as compared to standard treatment with heparin. A longer follow-up period is warranted to confirm the beneficial effects observed at 30 days with abciximab in this setting.

Abciximab↗
PubMed1999

Diagnostic value of exercise electrocardiography for predicting a positive scintigraphic test in patients with complete right bundle branch block.

BACKGROUND: The diagnostic value of exercise electrocardiography (ECG) in patients with complete right bundle block (cRBBB) remains controversial. The aim of this study was to investigate the diagnostic accuracy of exercise ECG for predicting ischemia in the presence of cRBBB. METHODS: From a series of 1300 consecutive patients attending for exercise ECG and 99mTc-tetrofosmin single photon emission computed tomography (SPECT), we identified 38 male patients with cRBBB and 38 matched controls with normal intraventricular conduction. Patients with left ventricular hypertrophy or previous revascularization were excluded. Exercise ECG (modified Bruce protocol) was considered positive at > or = 1 mm ST horizontal or downsloping depression in > or = 2 adjacent leads. SPECT imaging at rest and post-exercise was performed at least 48 hours apart. RESULTS: The odds ratio for ischemia comparing patients with positive and negative exercise ECGs was 11.0 (95% confidence interval 2.49-48.64, p = 0.002) in controls and 2.49 (95% confidence interval 0.64-9.08, p = 0.32) in cRBBB. The prior probability of ischemia was 0.37 in controls and 0.58 with cRBBB. The posterior probability after a positive test was 0.65 in controls and 0.68 in cRBBB. Thus, the utility of the test (posterior probability minus prior probability) was greater in controls (+0.28) than in cRBBB (+0.1). This difference was most pronounced in the anterior leads V1-V4 (controls +0.63 vs cRBBB +0.01) but less significant in the lateral leads V5-V6 (controls +0.26 vs cRBBB +0.21). Similar analysis also indicated reduced diagnostic value of negative exercise ECGs in cRBBB patients. CONCLUSIONS: The diagnostic value of exercise ECG is reduced in patients with cRBBB, although ST-segment changes in the lateral ECG territory provide superior predictive accuracy to those in the anterior leads. The use of SPECT as a first-line investigation may be justified in patients with cRBBB.

Aged↗
PubMed1998

Interleukin-10 differentially modulates MHC class II expression by mesangial cells and macrophages in vitro and in vivo.

Inhibition of major histocompatibility complex (MHC) class II expression by macrophages is the primary mechanism by which interleukin-10 (IL-10) exerts immune suppression. Little, however, is known of the effects of IL-10 on other types of cells which can be induced to express MHC class II during an inflammatory response. We therefore studied the effects of IL-10 treatment on the expression of MHC class II molecules in a rat model of immunologically induced glomerulonephritis. MHC class II mRNA levels in whole kidney were increased in saline-treated (control) animals with glomerulonephritis (2.6-fold increase versus normal, P = 0.028) and this was partially inhibited by treatment with IL-10 (P = NS). Double immunostaining of tissue sections was used to compare MHC class II expression by infiltrating macrophages and resident glomerular cells. IL-10 treatment reduced the proportion of glomerular macrophages which expressed detectable MHC class II (70% reduction, P = 0.03). In contrast, IL-10 treatment was associated with an increase in the number of resident glomerular cells expressing MHC class II, particularly within mesangial areas. Therefore, the effects of IL-10 on macrophages and mesangial cells were compared in vitro. IL-10 reduced constitutive MHC class II mRNA and cell surface expression by peritoneal macrophages. In contrast, IFN-gamma-stimulated mesangial cells (1097 cell line) cultured with IL-10 for 24 hr showed increased MHC class II mRNA (26% increase) and surface expression (72% increase in percentage MHC II+ by flow cytometry, P = 0.04) as compared with cells stimulated with IFN-gamma alone. IL-10 also directly up-regulated expression of ICAM-1 by 1997 cells. In conclusion, IL-10 was found to have contrasting effects on the production and cell surface expression of MHC class II molecules by mesengial cells and by macrophages, both in vitro and in vivo. The implications of these findings for IL-10-mediated immunosuppression are discussed.

Animals↗
PubMed1998

[Significance of electrocardiographic projection of ST-segment depression during exercise test in the prediction of the location of regional myocardial ischemia].

There is still some controversy whether ST segment depression during exercise testing might predict the location of myocardial ischemia. From a population of 1196 patients who underwent myocardial 99mTc-tetrofosmin exercise SPECT scintigraphy, 22 consecutive patients (20 males and 2 females, mean age 54 +/- 10 years) with no previous myocardial infarction, positive exercise testing (> or = 1 mm ST segment depression) performed in pharmacologic wash-out and angiographically documented isolated single vessel coronary artery disease (> or = 70% diameter stenosis in a main coronary artery) were selected. None of the patients showed > or = 1 mm ST segment depression exclusively in inferior leads (II-III-aVF). Eight patients (36%) showed > or = 1 mm ST segment depression exclusively in precordial leads (Group 1). The remaining 14 patients (64%) showed > or = 1 mm ST segment depression in both inferior and precordial leads (Group 2). No differences between groups were observed regarding peak exercise test parameters such as heart rate (124 +/- 28 vs 135 +/- 21 b/min, NS), rate-pressure product (22592 +/- 5323 vs 23118 +/- 4197 mmHg x b/min, NS) and exercise time (14.5 +/- 3.9 vs 15.1 +/- 2.9 min, NS) and the number of stress-induced reversible and partially reversible defects (3.3 +/- 3.4 vs 4.6 +/- 2.8, NS). All reversible and partially reversible defects were seen in the related coronary artery stenosis region. Among Group 1, 5 patient (62.5%) showed a > or = 70% stenosis of left descending coronary artery, 1 patient (12.5%) of left circumflex and 2 patients (25%) of right coronary artery. Similarly, among Group 2, 9 patients (64.3%) showed a significant stenosis of left descending coronary artery, 1 patient (7.1%) of left circumflex and 4 patients (28.6%) of right coronary artery. Thus, we were not able to show a relation between exercise ST segment depression and the location of myocardial ischemia as assessed by myocardial 99mTc-tetrofosmin SPECT scintigraphy in a population of patients selected on the basis of single coronary artery disease.

Adult↗
PubMed1998

[Safety, feasibility and efficacy of a new single-wire stent in the treatment of complex coronary lesions: the angiostent].

The angiostent is a single wire, flexible, highly radiopaque, balloon expandable stent. To evaluate the feasibility and safety of the deployment of this new stent, we report the clinical and procedural results of 70 procedures performed in 51 native coronary arteries of 48 patients, with objective evidence of ischemia. The target lesion was located in the left anterior descending artery in 18 (36%) cases, in the circumflex artery in 16 (31%) cases and in the right coronary artery in 17 (33%) cases. Mean reference vessel diameter was 3.2 +/- 0.4 mm and the minimal luminal diameter was 0.4 +/- 0.3 mm, with a mean diameter stenosis of 86 +/- 10%. Type B2 and C lesions were encountered in 56% of the cases. More than one angiostent was implanted in 14 vessels and multiple stenting was accomplished with the use of different stents in 8 coronary arteries. No major complications were reported. The post-procedural minimal luminal diameter was 3.2 +/- 0.4 mm with a mean diameter stenosis of 1.4 +/- 3.7%. In 25 cases (49%) major side branches raised from the stented segment and in all but one remained patent. In conclusion, the implantation of the angiostent is safe, feasible and effective, as it can be easily deployed at the lesion site, used for the treatment of complex lesions and preserves the patency of jailed side-branches.

Anticoagulants↗
PubMed1997

CD44 and hyaluronan expression in the development of experimental crescentic glomerulonephritis.

CD44 is a widely expressed cell surface glycoprotein which is involved in both cell-matrix and cell-cell interactions which regulate a variety of processes, including leucocyte migration and activation. Therefore, we examined the expression of CD44, and its major ligand hyaluronan, during the induction and progression of experimental glomerulonephritis. Antibody staining of normal rat kidney showed constitutive CD44 expression by resident glomerular macrophages, parietal epithelial cells, medullary and occasional cortical tubules. There was a marked increase in CD44 expression over days 1, 7 and 21 of rat crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Infiltrating monocytes and lymphocytes were CD44+, with ultrastructural studies showing high levels of CD44 expressed on the surface of lymphocytes adherent to activated endothelium. Marked hyaluronan deposition was seen in areas of fibrosis on days 7 and 21, such as glomerular crescents and the periglomerular area. Hyaluronan deposition was accompanied by the presence of many CD44+ cells. Double immunohistochemistry showed that both CD44+ED1+ macrophages and CD44+ myofibroblasts (identified by expression of alpha-smooth muscle actin) were present in areas of fibrosis. There was also a dramatic increase in cortical tubular CD44 expression, which was most evident in areas of tubular damage. Although tubular epithelial cells expressed CD44 upon both the basolateral and luminal surface, CD44 expression was most prominent within tightjunctions, suggesting a role for CD44-CD44 interactions in cell-cell adhesion within the tubule. Analysis of CD44 isoforms by reverse transcriptase-polymerase chain reaction (RT-PCR) showed that the standard form of CD44 predominated in both normal and diseased kidney. However, a series of alternatively spliced CD44 isoforms was also detected, whose expression was markedly increased during disease. At least seven isoforms containing the v6 domain were identified, with the smallest form representing activated T cells. In conclusion, CD44 is constitutively expressed in normal kidney and is dramatically up-regulated in rat anti-GBM disease, suggesting possible roles for the CD44-hyaluronan interaction in leucocyte recruitment, renal fibrosis and tubular cell-matrix and cell-cell interactions during the induction and progression of crescentic glomerulonephritis.

Animals↗
PubMed1997

Intrinsic renal cells are the major source of interleukin-1 beta synthesis in normal and diseased rat kidney.

BACKGROUND: A number of studies have demonstrated a pathological role for interleukin-1 (IL-1) in experimental models of glomerulonephritis, but the cellular pattern of renal IL-1 production remains poorly characterized. The aim of this study, therefore, was to identify the cell types expressing IL-1 in normal and diseased rat kidney. METHODS: Renal IL-1 beta expression was examined in normal rats and during a 21-day time course of rat accelerated anti-GBM glomerulonephritis by northern blotting, in situ hybridization and double immunohistochemistry. RESULTS: Interleukin-1 beta mRNA expression was readily detectable in normal rat kidney by northern blot analysis and in situ hybridization. Immunohistochemistry staining demonstrated constitutive IL-1 beta expression by glomerular endothelial cells and cortical tubular epithelial cells. There was a marked increase in whole kidney IL-1 beta mRNA in rat anti-GBM glomerulonephritis. Glomerular IL-1 beta immunostaining was upregulated, being expressed by podocytes, mesangial cells and infiltrating macrophages, and was particularly prominent within glomerular crescents. Double staining with the ED1 antibody showed IL-1 beta expression in up to 13% of glomerular macrophages, whereas 48% of macrophages within crescents stained for IL-1 beta. However, the most marked increase in IL-1 beta expression was seen in cortical tubular epithelial cells, particularly in areas of tubular damage. In situ hybridization confirmed that tubular IL-1 beta staining was due to local cytokine synthesis rather than protein absorption. CONCLUSIONS: This study has identified constitutive IL-1 beta expression by glomerular endothelium and tubular epithelial cells in normal rat kidney. In addition, the marked upregulation of IL-1 beta expression by intrinsic glomerular cells and tubules in rat anti-GBM disease suggests an important role for these cells in IL-1 dependent crescent formation and tubulointerstitial injury.

Animals↗
PubMed1997

Interleukin-10 is a mesangial cell growth factor in vitro and in vivo.

Macrophages are involved in the pathogenesis of mesangioproliferative glomerulonephritis. As macrophages are known to produce interleukin-10 (IL-10), we investigated the effect of recombinant murine IL-10 (rIL-10) on mesangial cell growth. In vitro studies were performed using the rat 1097 mesangial cell line. These cells exhibited a dose-dependent proliferative response to rIL-10 (23% to 70% increases at 80 ng/mL; p < 0.01), as assessed by both 3H-thymidine uptake and cell count. This effect was inhibited by preincubation of rIL-10 with a neutralizing anti-IL-10 antibody. When added to cultures of growth-arrested 1097 cells, IL-10 induced dose-dependent proliferation that paralleled the effects of platelet-derived growth factor. Incubation with a neutralizing anti-IL-10 Ab for 48 hours reduced 3H-thymidine uptake (median, 27% decreases; range, 2% to 56% decreases) versus a control Ab; p < 0.05). Rat mesangial cells were also shown to express IL-10 mRNA and protein, as determined by Northern blotting and immunostaining, thereby suggesting a role for IL-10 in autocrine mesangial cell growth. To examine the effects of IL-10 in vivo, inbred male Sprague-Dawley rats were given subcutaneous rIL-10 (0.5 mg/kg) for 3 (n = 6), 7 (n = 3), or 14 days (n = 4), or vehicle control, then killed. IL-10 administration induced a transient reduction in creatinine clearance of 35% at Day 3 (p < 0.01). Following IL-10 administration, an increase in glomerular cellularity was seen, which was maximal at Day 3 (82.7 +/- 5.9 nuclei/glomerular cross section versus control 64.6 +/- 4.6, 28% increases; p < 0.001) and maintained at Day 14 (23% increases; p < 0.01). Immuno-histochemical staining for proliferating cell nuclear antigen demonstrated an increased number of proliferating cells per glomerular cross section at day 3 (48% increases versus controls; p < 0.05). Staining for alpha-smooth-muscle actin showed significant labeling only in the glomeruli of IL-10-treated animals; double-labeling with an anti-proliferating cell nuclear antigen Ab demonstrated that some of these mesangial cells were proliferating. Collectively, these results suggest that IL-10 is a growth factor for rat mesangial cells both in vitro and in vivo.

Actins↗
PubMed1996

De novo CD44 expression by proliferating mesangial cells in rat anti-Thy-1 nephritis.

CD44 is the major cell-surface receptor for hyaluronan, and cell-matrix interactions mediated by the CD44/hyaluronan receptor-ligand pair are involved in a variety of cellular functions, including cell migration. The aim of the study presented here was to examine the expression of CD44 and hyaluronan in the mesangial proliferative response in rat anti-Thy-1 nephritis. In normal rat kidney, CD44 is expressed by medullary tubules, some distal tubules and thick ascending limbs of Henle, dendritic-like cells around Bowman's capsule, and some interstitial cells. However, only occasional CD44+ cells were found within the glomerular tuft. In experimental nephritis, there was an early glomerular influx of CD44+ macrophages, which peaked on Day 4 after anti-Thy-1 antibody injection. A striking finding was de novo CD44 expression by mesangial cells. This CD44 expression was restricted to the transient period of mesangial cell proliferation as shown by double-staining with an antibody against the proliferating cell nuclear antigen. Immunohistochemistry staining also demonstrated hyaluronan deposition within segmental areas of proliferating CD44+ cells, suggesting a functional interaction between the CD44/hyaluronan receptor-ligand pair during mesangial cell proliferation. In vitro, rat mesangial cells were shown to express mRNA and protein for the 90-kd isoform of CD44. In addition, hyaluronan-dependent aggregation of CD44+ mesangial cells was specifically inhibited by an anti-CD44 antibody, demonstrating a functional interaction between hyaluronan and the CD44 expressed on the surface of rat mesangial cells. In conclusion, these data suggest that cell-matrix interactions mediated by the CD44/hyaluronan receptor-ligand pair are involved in mesangial cell proliferation in rat anti-Thy-1 nephritis.

Animals↗
PubMed1996

[The immediate and midterm results of percutaneous mitral valvuloplasty in subjects over 60].

We have analyzed the immediate and mid-term (1 and 2 years) results of percutaneous mitral valvuloplasty (PMV) by Inoue's catheter in 97 patients < 60 years (Group A) compared with 34 patients > 60 years (Group B). In 61% Group A the patients were in NYHA functional class II, 36% in III, and 3% in I; in Group B, 56% of the patients were in NYHA functional class III, 38% in II, and 6% in IV. Mean mitral valve area was 1.1 cm2 before dilatation in both groups, and a significant (p < 0.0001) increase was obtained in both Group A (0.9 +/- 0.3 cm2) and Group B (0.8 +/- 0.3 cm2). No significant differences were observed between the two groups. Mean transvalvular gradient decreased significantly (p < 0.0001) from 13.6 +/- 5.7 to 7.2 +/- 3.1 mmHg in Group A, and from 9.9 +/- 4 to 6.5 +/- 2.3 mmHg in Group B (A vs B: p < 0.02). Optimal result was obtained in 94% and 88% of Group A and Group B patients, respectively. Suboptimal result was obtained in 2% and 6% of Group A and Group B patients, respectively. These differences were not significant. Failure of PMV occurred in 4% and 6%, respectively. At 1-year follow-up Group A 7 patients and 5 Group B patients showed restenosis; at 2-year follow-up one more restenosis was present in Group A (A vs B at 1 and 2 years: NS). We conclude that PMV is a safe and effective technique in young patients and in patients > 60 years.

Adult↗
PubMed1995

Deoxyspergualin inhibits mesangial cell proliferation and major histocompatibility complex class II expression.

It has previously been shown that the immunosuppressive drug deoxyspergualin can inhibit renal injury in experimental glomerulonephritis. This study examined whether deoxyspergualin can modulate the mesangial cell response to glomerular injury. Antiglomerular basement membrane glomerulonephritis was induced in primed rats. Groups of five animals were treated with deoxyspergualin (5 mg/kg per day) or saline from Day 0 until being euthanized on Day 1, 7, 14, or 21. Deoxyspergualin treatment significantly inhibited mesangial cell proliferation (proliferating cell nuclear antigen expression) over the disease course as assessed by double immunohistochemistry staining (P < 0.001 versus saline treated) and reduced glomerular major histocompatibility complex (MHC) class II expression. To demonstrate if this was a direct action of deoxyspergualin, an in vitro system was studied. The addition of deoxyspergualin caused a time- and dose-dependent inhibition of [3H]thymidine uptake by cultured rat mesangial cells. Of particular interest was the finding that deoxyspergualin inhibited the de novo cell surface expression of MHC class II antigens after interferon-gamma stimulation. However, deoxyspergualin did not prevent the cytoplasmic accumulation of MHC class II molecules, indicating that the drug interfered with a posttranslational event in MHC class II processing and/or assembly. Deoxyspergualin was not a general inhibitor of mesangial cells, and it had no effect on constitutive or lipopolysaccharide-induced transforming growth factor beta 1 expression. In conclusion, deoxyspergualin has been shown to inhibit the mesangial cell response to glomerular injury. This novel mode of action may provide an additional therapeutic benefit in the treatment of proliferative forms of glomerulonephritis.

Animals↗