ZeroExpander® effectiveness assessment in PEEK or PA12 in a group of paediatric patients with transverse maxillary deficiency.

AIM: The aim of this article is to compare the performance of ZeroExpander® realised using PEEK or PA12 for the expansion of the maxilla in paediatric patients, exploring a new concept for approaching maxillary expansion with a metal-free fixed automatic appliance, based on pre-programmed set-up and anchored on deciduous teeth. MATERIALS: It is a retrospective comparative study with a sample of 40 children in early or mixed deciduous dentition and transversal maxillary deficit, 20 treated with ZeroExpander® in PEEK and 20 treated with ZeroExpander® in PA12 with a mean age of 7.3 years old. The intraoral scans at T0 and at the end of the expansion were all performed by the same operator to obtain digital models on which were performed measurements by two other different operators. A descriptive analysis was conducted using frequencies and percentages for nominal variables and means and standard deviations for continuous variables. CONCLUSION: In cases of allergy or hypersensitivity to metals or to specific chronic or acute pathological conditions, which may require periodic magnetic resonance imaging (MRI), it may not be possible to use traditional and metal fixed expansion devices. Moreover the concept of autonomous driving in paediatric orthodontics is not only possible, but it is and will be more real and very useful in the future. The "ortho-paediatric dentistry concept" will increase the range of benefits for children and their families which, in addition to care and thanks to technology, demand well-being, safety, comfort and quality of life beyond clinics.

Modes and Mechanisms of Pacific Decadal-Scale Variability.

The modes of Pacific decadal-scale variability (PDV), traditionally defined as statistical patterns of variance, reflect to first order the ocean's integration (i.e., reddening) of atmospheric forcing that arises from both a shift and a change in strength of the climatological (time-mean) atmospheric circulation. While these patterns concisely describe PDV, they do not distinguish among the key dynamical processes driving the evolution of PDV anomalies, including atmospheric and ocean teleconnections and coupled feedbacks with similar spatial structures that operate on different timescales. In this review, we synthesize past analysis using an empirical dynamical model constructed from monthly ocean surface anomalies drawn from several reanalysis products, showing that the PDV modes of variance result from two fundamental low-frequency dynamical eigenmodes: the North Pacific-central Pacific (NP-CP) and Kuroshio-Oyashio Extension (KOE) modes. Both eigenmodes highlight how two-way tropical-extratropical teleconnection dynamics are the primary mechanisms energizing and synchronizing the basin-scale footprint of PDV. While the NP-CP mode captures interannual- to decadal-scale variability, the KOE mode is linked to the basin-scale expression of PDV on decadal to multidecadal timescales, including contributions from the South Pacific.

Excimer laser technology in percutaneous coronary interventions: Cardiovascular laser society's position paper.

Excimer Laser Coronary Atherectomy (ELCA) is a well-established therapy that emerged for the treatment of peripheral vascular atherosclerosis in the late 1980s, at a time when catheters and materials were rudimentary and associated with the most serious complications. Refinements in catheter technology and the introduction of improved laser techniques have led to their effective use for the treatment of a wide spectrum of complex coronary lesions, such as thrombotic lesions, severe calcific lesions, non-crossable or non-expandable lesions, chronic occlusions, and stent under-expansion. The gradual introduction of high-energy strategies combined with the contrast infusion technique has enabled us to treat an increasing number of complex cases with a low rate of periprocedural complications. Currently, the use of the ELCA has also been demonstrated to be effective in acute coronary syndrome (ACS), especially in the context of large thrombotic lesions.

Use of loupes magnification and microsurgical technique in thyroid surgery: ten years experience in a single center.

AIM: The use of microsurgical technique and loupes magnification as a support to traditional surgery can help surgical performance and prevent complications in thyroid surgery. PATIENTS AND METHODS: Between January 2004 and December 2014, 782 patients with thyroid diseases were operated by our team with microsurgical technique and loupes magnification 4.5x. All patients had pre and postoperative vocal cords assessment and calcemia and the collected data were analysed. RESULTS: Among the 782 patients, only six patients (0.77%) had unilateral vocal fold immobility treated with medical therapy, phoniatric and neck physiotherapy. All six patients showed complete laryngeal recovery of motility 6/8 weeks after treatment. There were not cases of permanent monolateral or bilateral vocal cord palsy. In 84 patients there were signs and symptoms of hypocalcemia. In 81 patients (10.36%) the restoring of biochemical parameters and the resolution of symptoms occurred between 2 and 6 weeks and in 3 cases (0.38%) there was permanent hypocalcemia more than six months. CONCLUSION: The use of microsurgical technique and loupes magnification in thyroid surgery are safety and effective procedures, that require an appropriate training in reconstructive microsurgery, but may significantly reduce post-operative complications. Here, we report for the first time the largest series of thyroid surgery performed with the use of microsurgical technique and loupes magnification, analysing the postoperative morbidity. In view of our results, we suggest the routine use of 4.5X loupes and microsurgical technique in thyroid surgery.

Long-term (12 to 18 months) functional voice assessment to detect voice alterations after thyroidectomy.

OBJECTIVES: Even when thyroidectomy preserves vocal cord motility it may leave patients with changes in voice quality. Although superior laryngeal nerve (LSN) damage after thyroidectomy manifests with aspecific symptoms, laryngoscopy discloses only slight morphological changes that are difficult to assess. We want to investigate the voice function in asymptomatic patients one year after thyroidectomy and to compare the obtained data against those of a healthy control group. PATIENTS AND METHODS: Thirty adult patients who had undergone thyroidectomy, all of them euphonic before and after the operation, were submitted to a complete voice assessment including voice self-evaluation tools, videolaryngostroboscopy and spectrographic analysis of voice. Primary outcome measures were differences between surgical patients and control group in terms of microperturbation of voice intensity and amplitude as measured by spectrographic analysis. RESULTS: In patients who had undergone thyroidectomy, acoustic parameters indicating amplitude microperturbations resulted slightly altered. All these values exceeded normal MDVP thresholds. Another interesting finding in our study sample concerns the lower F0 values we recorded in women patients after surgery than in healthy controls. Voice alterations may reflect prelaryngeal muscle scarring or fibrosis. Consider the possible alterations of vocal quality caused by scarring after surgery therefore strongly recommend surgery when the situation allows it, not to dissect the prelaryngeal muscles but only to spread apart. CONCLUSIONS: Our study conducted at least one year after thyroid surgery underlines that surgery-related slight voice deficits can persist over time. More refined phoniatric testing discloses voice alterations that normalize without specific rehabilitation therapy, therefore confirming that certain acoustic changes are clinically unimportant.

Secondary prevention of latex allergy in children: analysis of results.

OBJECTIVE: Latex allergy has become an increasing and clinically important problem. Several recommendation for secondary preventive measures have been advised. The aims of the study were to illustrate the results of the latex-safe protocol and to evaluate in allergic patients the role of risk factors for the development of latex allergy. METHODS: Latex-safe treatment was divided into the following phases: anamnestic identification, allergologic assessment, patient selection, intervention programme, preventive medication, operating room equipment, postoperative management, patient and family training, follow-up. RESULTS: Between 1998 and 2004, 6.832 patients underwent 7.333 operations. Anamnestic and diagnostic tests showed that 26 patients had latex allergy. 44 secondary perioperative latex-safe management have been accomplished in 26 children. No allergic event or complications linked to the procedure occurred. Atopy, congenital malformations frequently associated with latex allergy and the presence of 5 or more surgical procedures were the major risk factors recognized. Six out of the 26 patients (23%) had only one risk factor (atopy). Twenty out of 26 children (77%) had several associated risk factors: 8 of them had simultaneously 9 of the 10 analysed risk factors. Our data shows that, the higher their number, the higher the gravity of the allergy. CONCLUSIONS: Although latex allergy is a limited phenomenon, it is nevertheless quite frequent within risk groups. Most patients have simultaneously many risk factors for the development of such an allergy, and the occurrence of several risk factors increases severity of the allergy. Latex-safe perioperative management offers guarantees of safety against latex allergy phenomena.

Effects of balloon injury on neointimal hyperplasia in streptozotocin-induced diabetes and in hyperinsulinemic nondiabetic pancreatic islet-transplanted rats.

BACKGROUND: The mechanisms of increased neointimal hyperplasia after coronary interventions in diabetic patients are still unknown. METHODS AND RESULTS: Glucose and insulin effects on in vitro vascular smooth muscle cell (VSMC) proliferation and migration were assessed. The effect of balloon injury on neointimal hyperplasia was studied in streptozotocin-induced diabetic rats with or without adjunct insulin therapy. To study the effect of balloon injury in nondiabetic rats with hyperinsulinemia, pancreatic islets were transplanted under the kidney capsule in normal rats. Glucose did not increase VSMC proliferation and migration in vitro. In contrast, insulin induced a significant increase in VSMC proliferation and migration in cell cultures. Furthermore, in VSMC culture, insulin increased MAPK activation. A reduction in neointimal hyperplasia was consistently documented after vascular injury in hyperglycemic streptozotocin-induced diabetic rats. Insulin therapy significantly increased neointimal hyperplasia in these rats. This effect of hyperinsulinemia was totally abolished by transfection on the arterial wall of the N17H-ras-negative mutant gene. Finally, after experimental balloon angioplasty in hyperinsulinemic nondiabetic islet-transplanted rats, a significant increase in neointimal hyperplasia was observed. CONCLUSIONS: In rats with streptozotocin-induced diabetes, balloon injury was not associated with an increase in neointimal formation. Exogenous insulin administration in diabetic rats and islet transplantation in nondiabetic rats increased both blood insulin levels and neointimal hyperplasia after balloon injury. Hyperinsulinemia through activation of the ras/MAPK pathway, rather than hyperglycemia per se, seems to be of crucial importance in determining the exaggerated neointimal hyperplasia after balloon angioplasty in diabetic animals.

Membrane-bound protein kinase A inhibits smooth muscle cell proliferation in vitro and in vivo by amplifying cAMP-protein kinase A signals.

cAMP-dependent protein kinase is anchored to discrete cellular compartments by a family of proteins, the A-kinase anchor proteins (AKAPs). We have investigated in vivo and in vitro the biological effects of the expression of a prototypic member of the family, AKAP75, on smooth muscle cells. In vitro expression of AKAP75 in smooth muscle cells stimulated cAMP-induced transcription, increased the levels of the cyclin-dependent kinase-2 inhibitor p27(kip1), and reduced cell proliferation. In vivo expression of exogenous AKAP75 in common carotid arteries, subjected to balloon injury, significantly increased the levels of p27(kip1) and inhibited neointimal hyperplasia. Both the effects in smooth muscle cells in vitro and in carotid arteries in vivo were specifically dependent on the amplification of cAMP-dependent protein kinase (PKA) signals by membrane-bound PKA, as indicated by selective loss of the AKAP75 biological effects in mutants defective in the PKA anchor domain or by suppression of AKAP effects by the PKA-specific protein kinase inhibitor. These data indicate that AKAP proteins selectively amplify cAMP-PKA signaling in vitro and in vivo and suggest a possible target for the inhibition of the neointimal hyperplasia after vascular injury.

8-chloro-cAMP inhibits smooth muscle cell proliferation in vitro and neointima formation induced by balloon injury in vivo.

OBJECTIVES: The aims of the present study were to assess 1) the effect of 8-C1-cAMP (cyclic-3'-5'-adenosine monophosphate) on vascular smooth muscle cell (VSMC) proliferation in vitro and 2) the efficacy of systemic administration of 8-C1-cAMP on neointimal formation after balloon injury in vivo. BACKGROUND: Neointimal formation after vascular injury is responsible for restenosis after arterial stenting. Recently, 8-C1-cAMP, a cAMP analogue that induces growth arrest, has been safely administered in phase I studies in humans. METHODS: The effect of 8-C1-cAMP on cell proliferation was first assessed on SMCs in vitro. To study the effects of cAMP in vivo, balloon injury was performed in 67 rats using a 2F Fogarty balloon catheter. RESULTS: The 8-C1-cAMP markedly inhibited VSMC proliferation in vitro, reduced protein kinase A (PKA) RIalpha subunit expression, and induced PKA RIIbeta subunit expression. In addition, 8-C1-cAMP reduced, in a dose-dependent manner, neointimal area and neointima/media ratio after balloon injury. The proliferative activity, assessed by proliferating nuclear cell antigen immunostaining, revealed a reduction of proliferative activity of VSMCs in vivo in the 8-C1-cAMP group. Moreover, the systemic administration of 8-C1-cAMP did not affect renal function, blood pressure and heart rate. CONCLUSIONS: We conclude that 8-C1-cAMP potently inhibits VSMC proliferation in vitro and reduces neointima formation by balloon injury in vivo after systemic administration. These data may have a clinical relevance in designing future strategies to prevent restenosis after arterial stenting and perhaps after percutaneous transluminal coronary angioplasty.

A new rat model of small vessel stenting.

OBJECTIVES: Restenosis is the major complication of coronary angioplasty and stenting. In addition, the small vessel diameter represents a major limitation to the wide use of the technology. The aim of this study was to assess the feasibility and the vascular response of stent deployment in rat small vessels. METHODS: In 40 Wistar rats (500-550 g) a Nir stent crimped on a 1.5 mm Comet angioplasty balloon catheter was deployed at high pressure in the common carotid artery. Neointimal area, neointima/media ratio and the arterial dimension were assessed immediately and at 7, 14, 21, and 28 days after stenting. RESULTS: After stent deployment, the neointimal area and the neointima/media ratio increased progressively and peaked at 14 days (p < 0.05 vs 0 and 7 days). Alpha-actin-positive cells were found circumferentially organized on the lumen surface. At 21 and 28 days after stenting, the neointima and the neointima/media ratio were not statistically different compared with the results obtained fourteen days after stent deployment. No significant differences in the area of external elastic lamina were observed during the study period. In contrast, the internal lumen area was reduced significantly at 14, 21, and 28 days after the stent deployment. Subacute thrombosis rate after stent implantation was 26.5 %. CONCLUSIONS: The results of this study demonstrated that the balloon expandable stents can be safely placed into rat arteries and the reduction of the internal arterial lumen observed after stent deployment was only due to the neointima formation whereas remodeling did not occur.

Effects of hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin on smooth muscle cell proliferation in vitro and neointimal formation in vivo after vascular injury.

OBJECTIVES: We sought to evaluate the effects of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on vascular smooth muscle cell (VSMC) proliferation in vitro and neointimal formation in vivo after vascular injury. BACKGROUND: Neointimal hyperplasia after vascular injury is responsible for restenosis after arterial stenting, whereas arterial remodeling and neointimal formation are the causes of restenosis after percutaneous transluminal coronary angioplasty. METHODS: We assessed the effect of simvastatin on in vitro VSMC proliferation. To study the effects of simvastatin in vivo, balloon injury and stent deployment were performed in the common carotid artery of rats. Neointimal area was measured two weeks later in the balloon injury model and three weeks after stent deployment. RESULTS: Simvastatin markedly inhibits VSMC proliferation in vitro. In vivo, simvastatin reduced, in a dose-dependent manner, the neointimal area and the neointima-media ratio after balloon injury from 0.266 +/- 0.015 mm2 to 0.080 +/- 0.026 mm2 and from 1.271 +/- 0.074 to 0.436 +/- 0.158 (p < 0.001 vs. control rats) at the highest dose. Simvastatin also significantly reduced the neointimal formation and the neointima-media ratio after stenting from 0.508 +/- 0.035 mm2 to 0.362 +/- 0.047 mm2 (p < 0.05 vs. control rats) and from 2.000 +/- 0.136 to 1.374 +/- 0.180 (p < 0.05 vs. control rats). The vessel thrombosis rate after stent deployment was 30% in the control group and 11.1% in the treated group (p = NS). Moreover, the systemic administration of simvastatin did not affect hepatic and renal functions, blood pressure or heart rate. CONCLUSIONS: Simvastatin potently inhibits VSMC proliferation in vitro and reduces neointimal formation in a rat model of vascular injury.

Activation of cAMP-PKA signaling in vivo inhibits smooth muscle cell proliferation induced by vascular injury.

Injury of the arterial wall induces the formation of the neointima. This structure is generated by the growth of mitogenically activated smooth muscle cells of the arterial wall. The molecular mechanism underlying the formation of the neointima involves deregulated cell growth, primarily triggered by the injury of the arterial wall. The activated gene products transmitting the injury-induced mitogenic stimuli have been identified and inhibited by several means: transdominant negative expression vectors, antisense oligodeoxynucleotides, adenovirus-mediated gene transfer, antibodies and inactivating drugs. Results of our study show that local administration of 3',5'-cyclic AMP and phosphodiesterase-inhibitor drugs (aminophylline and amrinone) to rats markedly inhibits neointima formation after balloon injury in vivo and in smooth muscle cells in vitro. The growth inhibitory effect of aminophylline was completely reversed by the inhibition of cAMP-dependent protein kinase A (PKA). These findings indicate an alternative approach to the treatment of diseases associated with injury-induced cell growth of the arterial wall, as stimulation of cAMP signaling is pharmacologically feasible in the clinical setting.

In vivo gene transfer: prevention of neointima formation by inhibition of mitogen-activated protein kinase kinase.

BACKGROUND: The mitogen-activated protein kinase kinase (MAPKK) is a protein downstream ras which is rapidly activated in cells stimulated with various extracellular signals. These proteins are believed to play a pivotal role in integrating and transmitting transmembrane signals required for cell growth. METHODS AND RESULTS: To study the effect of inhibition of MAPKK on smooth muscle cell (SMC) proliferation in vivo after vascular injury, we performed experimental balloon angioplasty using the standard Clowes technique in male Wistar rats 14-weeks old. The animals did not receive any treatment after vascular injury (N = 6) or were randomly assigned to receive, after balloon injury, a 30% (w/v) pluronic gel solution applied to the injured carotid artery, containing respectively: 1) no plasmid DNA (n = 10); 2) RSV-lacZ (encoding the beta-galactosidase gene) as control gene without effects on SMC proliferation (n = 10); 3) Tg-CAT (encoding cloramphenicol acetyl-transferase gene under the control of thyreoglobulin promoter) as an additional control gene without effects on SMC proliferation (n = 7): 4) a negative mutant of Mitogen-Activated Protein Kinase Kinase (MAPKK-) (n = 13). Fourteen days after vascular injury, carotid arteries were removed and cross sections were cut and stained with hematoxylin/eosin. Morphometric analysis demonstrated, in the MAPKK- treated rats, a significant reduction of both neointima (0.096+/-.018 mm2 vs. 0.184+/-0.019 mm2, p < 0.01) and neointima/media ratio (0.603+/-0.103 vs. 1.471+/-0.161, p < 0.01) compared to control DNA. CONCLUSIONS: The inhibition of MAPKK, by a dominant inhibitor mutant gene, prevents the SMC proliferation after vascular injury in vivo.

Inotropic stimulation by dobutamine increases left ventricular regional function at the expense of metabolism in hibernating myocardium.

The mechanism by which dobutamine increases the contraction of chronically dysfunctional myocardium and its effects on metabolism are still unknown. The aim of this study was to assess regional myocardial metabolism at rest and during an intracoronary dobutamine infusion in patients with hibernating myocardium. Eleven asymptomatic patients with single proximal stenosis of the left anterior descending coronary artery and persistent left ventricular dysfunction at rest (undergoing percutaneous transluminal coronary angioplasty [PTCA]) were studied prospectively. Regional left ventricular function was assessed by two-dimensional (2D) echocardiography and regional perfusion by thallium-201 single-proton-emission computed tomography. Great cardiac vein and aortic blood samples were obtained for measurements of lactate and plasma free fatty acid (FFA) concentrations. Inotropic challenge, obtained by using intracoronary dobutamine infusion, increases regional left ventricular function. However, the arteriovenous AV lactate difference was 0.206 = 0.070 mmol/L at rest, and it decreased to 0.018 = 0.069 mmol/L (p < 0.05 vs baseline) and 0.066 = 0.068 mmol/L (p < 0.05 vs baseline) at 4 and 10 minutes of dobutamine infusion, respectively. Thus the hibernating myocardium does not produce lactate at rest. However, when regional contraction is stimulated, dobutamine-induced inotropic challenge may cause a perfusion-contraction mismatch with an activation of anaerobic glycolysis.

Smooth muscle cell proliferation is proportional to the degree of balloon injury in a rat model of angioplasty.

BACKGROUND: A variable degree of smooth muscle cell (SMC) proliferation after balloon injury has been reported in previous rat studies. It is unknown whether balloon injury induces c-fos expression and whether it is related to the degree of vascular injury in vivo. Therefore, we tested the hypothesis that proportional increases in neointimal formation and c-fos expression might be present after different degrees of balloon dilation. METHODS AND RESULTS: Angioplasty of the carotid artery was performed with a balloon catheter. Vascular injury was evaluated at 0, 0.5, 1.0, 1.5, and 2 atm (n = 6 for all). In 40 additional rats, total RNA dot blots were performed to assess the effect of various degrees of balloon injury on c-fos expression. SMC proliferation proportional to the increases of inflation pressure was found between 0 and 2 atm with neointimal areas of 0.002 +/- 0.002, 0.069 +/- 0.014, 0.128 +/- 0.043, 0.190 +/- 0.010, and 0.255 +/- 0.041 mm2, respectively. When the degree of SMC proliferation (neointima and neointima/media ratio) was plotted against balloon inflation pressure, a linear relation was observed (r = .733, P < .001 and r = .755, P < .001, respectively). An increase in c-fos expression proportional to the degree of injury was found 30 minutes after injury. CONCLUSIONS: Neointimal proliferation produced by balloon injury is related to balloon inflation pressure, supporting the concept of an SMC proliferative response proportional to the degree of injury. The increase in SMC proliferation is associated with a proportional increase in the early expression of the c-fos nuclear proto-oncogene.

Inhibition of cellular ras prevents smooth muscle cell proliferation after vascular injury in vivo.

Proliferation of smooth muscle cells of the arterial wall in response to local injury is an important aetiologic factor of vascular proliferative disorders such as atherosclerosis and restenosis after angioplasty. Ras proteins are key transducers of mitogenic signals from membrane to nucleus in many cell types. We investigated the role of ras proteins in the vascular response to arterial injury by inactivating cellular ras of rats in which the common carotid artery was subjected to balloon injury. DNA vectors expressing ras transdominant negative mutants, which interfere with ras function, reduced neointimal formation after injury. Our results indicate a key role for ras in smooth muscle cell proliferation and show that the local delivery of transdominant negative mutants of ras in vivo might prevent some of the acute vascular injury caused by balloon injury.

[Gene therapy for the treatment of restenosis after coronary angioplasty]. / Terapia genica per il trattamento della ristenosi dopo angioplastica coronarica.

Accumulation and proliferation of vascular smooth muscle cells are associated with atherosclerosis and hypertension. Proliferation of smooth muscle cells constitutes a major pathological event responsible for long-term failure of coronary and peripheral arterial bypass graft as well as the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA). The incidence of restenosis after PTCA has been reported to be as high as 40-45% within 3-6 months. Major advantages in recombinant deoxyribonucleic acid (DNA) technology and eukaryotic gene regulation allow to hypothesize gene therapy as a potential treatment for inherited and acquired diseases. Gene therapy is the introduction of genes into somatic cells to correct an inherited or acquired disorder through the synthesis of missing or defective protein. Although no disease has yet been treated by gene therapy, several gene transfer protocols have recently been undertaken. We have studied the expression of foreign DNA that has been introduced into smooth muscle cells after balloon carotid injury in a rat model of angioplasty. The effects of different degree of balloon injury on neointima formation and c-fos expression was also assessed. Our data demonstrate that site-specific gene expression can be achieved by direct gene transfer in vivo and could be applied to the treatment of restenosis after PTCA.

Coronary artery vasoconstriction after successful single angioplasty of the left anterior descending artery.

Percutaneous transluminal coronary angioplasty is associated with spontaneous transient vasoconstriction. The mechanisms by which coronary vasoconstriction occurs distally to a successful dilated stenosis after coronary artery angioplasty are still unknown. The present study was planned to investigate the effect of successful coronary artery angioplasty on coronary vasomotion distal to a dilated stenosis and in the control vessel and the role of alpha-adrenergic receptors on coronary vasomotion after successful coronary artery angioplasty. We prospectively studied 32 consecutive patients scheduled for elective single coronary artery angioplasty of the left anterior descending coronary artery. Only aspirin, 325 mg, or nitroglycerin was allowed in the week before the study; no premedication with diazepam or other drugs was given. In group 1 (control patients, n = 20), quantitative coronary angiography was performed in the control state; 5 and 15 minutes after coronary artery angioplasty; and after intracoronary nitroglycerin infusion, 300 micrograms. In group 2 (n = 12), intracoronary phentolamine, 2 mg, was infused regionally through the balloon catheter before the coronary artery angioplasty, and coronary angiography was performed at baseline, 15 minutes after balloon deflation, and after nitroglycerin infusion. In group 1, constriction of the coronary segment distal to a dilated stenosis (2.4 +/- 0.8 to 2.1 +/- 0.6 mm, -14.6% vs baseline; p < 0.05) and of the circumflex coronary artery segment (2.8 +/- 0.7 to 2.5 +/- 0.6 mm, -10.7% vs baseline, p < 0.05) occurred 15 minutes after coronary artery angioplasty. The degree of vasoconstriction was not correlated with the lesion severity before coronary artery angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Purification of interferon gamma-interferon gamma receptor complexes by preparative electrophoresis on native gels.

Cytokine-receptor complexes are required for certain studies including crystallization, NMR spectra, and investigation of the biological response mechanism to the cytokine. The purity of the ligand-receptor complex is critical for most of these applications. We investigated the possibility of purifying protein-protein complexes by electrophoresis on native gels. Starting with partially purified mouse and highly purified human proteins, we prepared milligram amounts of interferon gamma-interferon gamma receptor complexes by preparative electrophoresis on nondenaturing polyacrylamide gels. In both cases, pure ligand-receptor complexes with the correct stoichiometry of binding were recovered. Electrophoresis on preparative native gels may prove to be of general interest for the preparation of protein-protein complexes to be used in diverse studies.