Viale Morgagni Research Articles

Tensor-product surface patches with Pythagorean-hodograph isoparametric curves

Tensor-product surface patches with Pythagorean-hodograph isoparametric curves Rida T. Farouki Department of Mechanical and Aerospace Engineering, University of California, Davis, CA 95616, USA. Francesca Pelosi Dipartimento di Matematica, Universit`a di Roma “Tor Vergata,” Via della Ricerca Scientifica, 00133 Roma, Italy. Maria Lucia Sampoli Dipartimento di Ingegneria dell’Informazione e Scienze Matematiche, Universit`a di Siena, San Niccol`o, Via Roma 56, 53100 Siena, Italy. Alessandra Sestini Dipartimento di Matematica e Informatica, Universit`a di Firenze, Viale Morgagni 67/A, 50134 Firenze, Italy. Abstract The construction of tensor–product surface patches with a family of Pythagorean–hodograph (PH) isoparametric curves is investigated. The simplest non–trivial instances, interpolating four prescribed patch boundary curves, involve degree (5, 4) tensor–product surface patches x(u, v) whose v = constant isoparametric curves are all spatial PH quintics. It is shown that the construction can be reduced to solving a novel type of quadratic quaternion equation, in which the quaternion unknown and its conjugate exhibit left and right coefficients, while the quadratic term has a coefficient interposed between them. A closed– form solution for this type of equation is derived, and conditions for

Use of biosimilars in hematopoietic stem cells transplantation

tation (HSCT); this procedure is by itself characterized by high cost and therefore there is a particular interest in mechanisms and procedures allowing to save costs. As such, HSCT procedure is currently monitored by complex mechanisms that involve scientific accreditation and surveillance operated by regulatory authorities. Information on marketing approval, extrapolation, labelling, substitution, immunogenicity and traceability of each biosimilar product is of importance particularly in the settings of HSCT where the outcome of patients is affected by an exceedingly large number of factors Correspondence: Alberto Bosi Hematology Unit A.O. Careggi and University of Florence Viale Morgagni, 85 50134 Florence, Italy E-mail: alberto.bosi@unifi.it

Can immigration solve the aging problem in Italy? Not really …

Immigration from the developing countries is beneficial for a rich, aging country. However, unless under extreme assumptions of very strong and temporary immigration of young guest workers (Gastarbeiter), its effects are modest and relatively short lived: after a while, immigrants too become older and retire; their fertility typically adapts rather quickly to the standards of the host country; and, in all cases, the share of foreigners increases very rapidly if immigrants must be a substitute for missing births. These intuitive considerations, here supported by the results of a set of simulations specifically tailored to the case of Italy, lead to the conclusion that immigration cannot counter aging, but only attenuate its extremes: structural adjustments, and fertility closer to replacement level, have no substitutes. Gustavo DE SANTIS, Full Professor of Demography, Department of Statistics "G. Parenti", University of Florence, Viale Morgagni, n. 59, 50134-Firenze, Italy. E-mail: desantis@ds.unifi.it .

A contribution for validation of ECG criteria for interatrial conduction delay

The electrophysiological phenomena related to AF are still incompletely understood, and despite the advances in pharmacological and non-pharmacological management of AF, we are far from being satisfied with the available treatment modalities and predictors of their success. Impaired interatrial conduction has been demonstrated in patients with AF [1], and it has been indicated that this condition can be associated with a reduced left atrial function [2]. In the intact human heart, conduction from the right atrium to the left atrium (LA) is known to occur through Bachmann bundle (BB), the posterior rim of fossa ovalis (FO), and the coronary sinus ostial region (CS) [3]. Impairment of interatrial conduction has been evaluated by ECG as prolongation of P wave duration or its morphology changes. Changes of P wave duration (>120 ms) andmorphology (+/−) in leads D3 and aVF have been utilized to indicate the existence of a conduction delay through Backmann bundle [4]. A +/−P-wave morphology in V1 has been advocated as expression of an interatrial conduction defect through the posterior rim of FO [3]. The latter interatrial delay can be further evidenced measuring P-wave terminal force (PTF), defined as product of the duration (D) by the amplitude (A) of the terminal phase of the P-wave in V1 [5]. The aim of our study was to furnish a contribution for verifying the diagnostic accuracy of these electrocardiographic criteria by comparison of ECG and electroanatomic mapping. Patients were studied just before catheter ablation of atrial fibrillation. At the time of electroanatomic mapping all patients were in sinus rhythm. A quadripolar diagnostic catheter was placed in the coronary sinus for time reference. Electroanatomic mapping was performed using the Carto system (Biosense Webster, Diamond Bar CA USA) with either a 7F Navistar or Thermocool catheter (Biosense Webster). ⁎ Corresponding author at: University of Florence, Department of Medical and Surgical Critical Care, Viale Morgagni 85, 50134 Florence, Italy. Tel.: +39 055 7947514. E-mail address: gemma@gmx.it (G. Filice). Fig. 3. Coronary angiography of the right internal thoracic artery “free” graft to the left anterior descending artery (A, B) after angioplasty of its proximal third (white arrow). Angiogram of the saphenous vein graft to a diagonal branch (C) shows the disappearance of the collateral circulation between the grafts (black arrow).

A 72-year-old man with intermittent fever, anemia and a history of coronary and peripheral artery disease

Dr. Del Pace: A 72-year-old man with history of coronary and peripheral artery disease was admitted to this hospital with fever, fatigue and loss of weight. He had hypertension, type 2 diabetes mellitus and hyperlipidemia. He suffered from an ischemic cardiomyopathy with a low ejection fraction (33%). Fifty years prior he had undergone subtotal gastroresection for peptic ulcer. Seventeen years prior to this current admission (PTA), he had an aortobifemoral bypass grafting for symptomatic peripheral artery disease, and 8 years prior he had a myocardial infarction. Three vessel coronary disease was detected and coronary-artery bypass grafting had been carried out. One year PTA, he experienced an episode of sustained ventricular tachycardia, treated with stenting of the anterior descending coronary artery, followed by an internal cardiac defibrillator (ICD) implantation. Ten months PTA, he had a massive enteric bleeding complicated by hemorrhagic shock. A colonoscopy revealed ulcerated cecal angiodysplasia that was treated with an application of metallic clips. During the following months, he was admitted several times for sideropenic anemia without evidence of acute gastrointestinal bleeding, and iron therapy was administrated. Two colonoscopies were performed but no source of active bleeding was detected. Two months PTA, he developed a low-grade fever resistent to a 2-week course of antibiotic therapy with levofloxacin. Laboratory tests showed a normocytic anemia (8.1 g/dL) with normal levels of B12 and folic acid, with low levels of sideremia (13 lg/dL), and a normal haptoglobin. An esophagogastroduodenoscopy was normal. Neoplastic markers (NSE, CA 125, CA 15-3, CA 72-4, CA 19-9, CYFRA 21-1, CEA, alfa-FP) were all in the normal range. Antinuclear antibody, ANCA, rheumatoid factor were negative as well as immunofixation in serum and urine. A computed tomography (CT scan) of the abdomen with contrast material confirmed ceacum angiodysplasia, but did not reveal active enteral bleeding. Transesophageal echocardiography was performed, and a vegetation on the ICD catheter was found. One blood culture was positive for Streptococcus intermedius. Treatment with amoxicillin was started, and during the hospital stay, the fever disappeared. Removal of the pacemaker was suggested, but the patient refused it. After discharge, he completed a 4-week cycle of antibiotic therapy, but after 1 week of withdrawal, fever developed again with malaise, fatigue and weight loss. He was readmitted to this hospital. On examination, the patient appeared in mild distress. He had low-grade fever (37.5 C). The Blood pressure was 100/50 mmHg, pulse rate 70 beats/min and oxygen saturation 98% while he was breathing ambient air. A grade 2/6 S. Del Pace A. Savino (&) G. F. Gensini Department of Heart and Vessels, Careggi Hospital, University of Florence, Viale Morgagni 85, 50139 Florence, Italy e-mail: savino.andrea@gmail.com

New evidence in pulmonary and preventive medicine

Chronic obstructive pulmonary disease (COPD) is increasing in prevalence and is usually associated with periodic exacerbations. Roflumilast is an oral anti-inflammatory agent. The efficacy and safety of the phosphodiesterase-4 inhibitor roflumilast have been investigated in studies of unselected patients with moderate-to-severe COPD. This article was aimed to investigate whether roflumilast reduces the frequency of exacerbations requiring corticosteroids in patients with moderate to severe COPD. Two placebo-controlled, double-blind, multicentre trials (M2-124 and M2-125) with identical design performed in two populations of outpatients with COPD older than 40 years, with severe airflow limitation [postbronchodilator forced expiratory volume in 1 s (FEV1) was 50% or less than the predicted value], bronchitic symptoms (chronic cough and sputum production), and a history of exacerbations (at least one recorded COPD exacerbation requiring systemic glucocorticosteroids or treatment in hospital, or both, in the previous year). Each trial had an initial 4-week run-in period, during which patients took a placebo once a day and recorded their use of shortacting bronchodilator drugs, and production of cough and sputum on their daily diary cards. Patients were then randomly assigned to oral Roflumilast 500 lg once a day or placebo for 52 weeks. Inhaled corticosteroid and longacting anticholinergic inhalators were not allowed. Patient recruitment began in February 2006, and the studies ended in July 2008. 1,523 patients and 1,568 were randomly assigned and treated, respectively, in the M2-124, and in M2-125 study. Change in prebronchodilator (FEV1) during treatment and the rate of COPD moderate or severe exacerbations were the primary endpoints. Analysis was by intention to treat. In the pooled analysis, in this study on patients with moderate to severe COPD prebronchodilator, FEV1 increased by 48 mL with roflumilast compared with placebo (p 0.001) and the estimated rate of exacerbations per patient per year was 17% lower in the roflumilast group than in the placebo group (p 0.003). Roflumilast improved measures of lung function in prebronchodilator and postbronchodilator period (FEV1, forced vital capacity, and peak expiratory flow) regardless of use of longacting b2 agonists. Patient withdrawal and adherence were similar in all groups. Mortality rate was not different in the different groups. The authors concluded that roflumilast reduced exacerbation rate and significantly improved lung function independently of the smoking status or concomitant medication. The authors outlined that this treatment is not suitable for all COPD patients since gastrointestinal effects or headache are more common in roflumilast group than in placebo group. B. Dilaghi (&) Emergency Department, Azienda Ospedaliera Universitaria Careggi, Viale Morgagni 85, 50134 Florence, Italy e-mail: beatrice.dilaghi@tin.it

Breaking news for the fifth year of Internal and Emergency Medicine

With this first issue of 2010 IEM is entering its fifth year of publication, and this is the fourth issue I have the honor to sign as Editor-in-Chief. As you can see, the Editorial Board has been renewed. Significant changes were introduced both in the composition and in the more general organization. First of all, we introduced a new Board in addition to the existing Internal Medicine and Emergency Medicine ones. The reason of this reorganization is to take advantage of a wider panel of experts in a broader range of subdisciplines of Internal Medicine. The new Board deals with Clinical Evidence and Health Technology Assessment and will be chaired by the past Editor-in-Chief, Gian Franco Gensini. He will be supported by the Deputy Editor Lorenzo Moja and the joining members. I wish these colleagues success achievements in their new endeavor. Significant changes have also been introduced in the composition of the Editorial Board of Emergency Medicine, with the introduction of new European and American members, and in that of Internal Medicine. Finally, the International Advisory Board has been reintroduced and includes past and new collaborators of our journal. I wish to thank the past President of the Italian Society of Internal Medicine (SIMI), Giuseppe Licata, the new President Francesco Violi, and all the members of past and new SIMI Council for providing me their support. A special thank goes to the Co-Editor Peter Rosen for his continuous and precious job in leading the Emergency Section of the journal. Good news from the Publisher! Usage of IEM articles increased five times from 2007 to 2008. Moreover, in the period January–September, the 2009 growth ratio of full-text downloads reached 27%. PubMed linkouts number represents the number of links from PubMed to SpringerLink full-texts; this tool helps to increase the visibility and content’s dissemination of our journal. Comparing the data related to the period January– August, PubMed linkouts increased by 46% from 2008 to 2009. During 2009 we received about 250 submissions which is a good result for a relatively new journal. Thomson Reuters-ISI will assign a 2009 Impact Factor. Unfortunately, a technical problem due to a late official communication, did not allow us to receive an Impact factor already in 2008. We will receive the official 2009 communication next summer. This will represent an important starting point for planning future development of the journal. A new section edited by Peter Rosen and named Medical Illustration, started in the second half of 2009. It gathered the interest of the readers and several papers have already been received over the last months, carefully selected by the Co-Editor. I wish to remind you to consult author instructions which have been changed over 2009 and to prepare manuscripts strictly following the instructions on the journal website (http://www.springer.com/medicine/internal/ journal/11739). Please note that review articles are usually prepared by invited experts but also unsolicited high quality Reviews can be considered for publication. The journal accepts D. Prisco (&) Editor-in-Chief, Internal and Emergency Medicine, Dipartimento di Area Critica Medico Chirurgica, Universita degli Studi di Firenze, Viale Morgagni 85, 50134 Florence, Italy e-mail: priscod@aou-careggi.toscana.it

Pulmonary arterial hypertension

In Internal and Emergency Medicine, Wu and coworkers [1] review the topic of pulmonary arterial hypertension. Overall, their article is sound and pertinent; however, some issues deserve comments. First, the value of chest radiography in the diagnostic process is somewhat overlooked. As pointed out by the authors, a prominent pulmonary artery trunk, or enlargement of the right heart cavities are strongly suggestive of pulmonary arterial hypertension. However, chest radiography also provides valuable information as regards chronic left heart failure, which is often associated with elevated pulmonary artery pressure. Chronic left heart failure is manifested on the chest radiograph by enlargement of the left heart cavities, dilated upper lobe vessels, and interstitial edema [2]. Therefore, chest radiography should be firmly incorporated in the diagnostic workup of suspected pulmonary arterial hypertension for it offers important clues to differentiate precapillary from post-capillary pulmonary hypertension. Transthoracic echocardiography is often inaccurate in estimating pulmonary artery systolic pressure (PASP). This is clearly borne out by a recent prospective study of 65 patients, suspected of having pulmonary arterial hypertension, who underwent Doppler echocardiography (DE) and right heart catheterization (RHC) within 1 h of the other test [3]. In that study, estimates of PASP by DE are considered ‘‘accurate’’ if they fall within 10 mmHg of the value measured by RHC. In the study, echocardiographic estimates of PASP could be rated accurately in only 48% of the patients, underestimation occurring in 25%, and overestimation in 27% [3]. There was a significant, positive correlation between DE estimates and actual measurements of PASP at RHC, with a correlation coefficient of 0.66. Nevertheless, the correlation coefficient is simply a measure of an association between two variables, and not of the agreement between two methods of measuring a given variable [4]. Failure to understand this, may lead to serious misconception of the value of any diagnostic method in clinical practice [4]. The inaccuracy of DE in estimating PASP is often due to a poor visualization of the tricuspid regurgitation jet, or because of an unreliable estimation of the right atrial pressure from the compressibility of the inferior vena cava [3]. Thus, even though echocardiography is a useful noninvasive screening tool, physicians should not be overly reliant on DE estimates of PASP in their approach to patients with suspected pulmonary arterial hypertension, or in assessing changes of PASP in response to therapy. Escalation therapy with dual or multimodal medication regimens is considered standard of care by current treatment guidelines for pulmonary hypertension [1]. In a recent cohort study, 821 patients with established pulmonary arterial hypertension received bosentan as the initial treatment, and were followed up to 3 years [5]. Of the 190 patients who died during follow-up, only 21 (11%) had been escalated to prostanoid therapy. The fact that 89% of the patients who expired did so without being escalated to prostanoids is of concern. Possible explanations of such an unexpected finding are: (a) inadequate characterization of patients at inclusion; (b) insufficient knowledge of treatment options by the prescribing physicians; (c) reluctance to adhere to treatment guidelines M. Miniati (&) Dipartimento di Area Critica Medico Chirurgica, Universita degli Studi di Firenze, Viale Morgagni 85, 50134 Florence, Italy e-mail: Massimo.Miniati@unifi.it

Out-of-hospital asystole caused by hanging treated with endovascular mild therapeutic hypothermia: a case report

Hanging may result in death either from direct, immediate damage to vital organs (spinal cord injury, airway disruption, carotid artery laceration), or from indirect effects on the cardiovascular system (autonomic reflex through the carotid sinus body compression, airway occlusion), with cardiac arrest representing the worst clinical complication [1]. Here we report a case of out-of-hospital cardiac arrest caused by hanging, which has been treated with mild therapeutic hypothermia by an endovascular technique, with complete neurological recovery. A 53-year-old man attempted suicide by hanging. The Mobile Pre-hospital Emergency Team was alerted by his wife, and arrived on the site 10 min after the event. At the scene, the medical team found the patient positioned on the floor in cardio-respiratory arrest (first cardiac rhythm detected was asystole). A cervical collar and an intravenous line were immediately put in place, and the Advanced Life Support protocol was started by the paramedics and the emergency physician on the scene. The patient was immediately intubated, artificially ventilated, and received epinephrine (2 mg) and atropine (1 mg). After 5 min of resuscitation, during which time the patient remained in asystole, the patient recovered a spontaneous cardiac sinus rhythm (heart rate 90 beats/ min), with an arterial blood pressure of 120/70 mmHg. The Glasgow Coma Scale (GCS) was 4, and pupil assessment was normal. The patient was transferred to the Trauma Center by Emergency Helicopter after medication with midazolam, morphine, atracurium. The patient was admitted to the ED 1 h after the event. An anesthesiologist from the Intensive Care Unit (ICU) was present at admission, and followed the patient during ED assessment, as provided in the internal protocol of the Trauma Center. A central venous oximetry catheter (PreSep, Edwards Lifesciences LLC, Irvine, CA, USA) was inserted in the right internal jugular vein, under the guide of a bedside ultrasonography, and a catheter for invasive arterial pressure monitoring (Leadercath, Vygon, Ecouen, France) was placed in the left femoral artery. A mean arterial pressure (MAP) above 65 mmHg, and a central venous oxygen saturation (CvO2 sat) above 70% was achieved with fluid [saline and 6% hydroxyethylstarch (HES 130/0.4)] infusions. After stabilization, the patient underwent a computerized tomography (CT)-scan of the head–neck–spinal vertebrae region, which demonstrated no encephalic alteration or traumatic dislocation of the cervical vertebrae, and was transferred to the ICU. On admission to the ICU, the patient had a GCS of 7. He presented myoclonus limited to the upper limbs. Empiric therapy for post-anoxic seizures was started with valproic acid which was maintained until discharge. After sedative (propofol and fentanyl) wash-out, we performed an electroencephalographic (EEG) examination that showed signs of post-anoxic cerebral distress, but no seizure-like electrical activity. Somatosensory evoked potentials (SEPs) did not show cortical–subcortical signal alterations. A mild therapeutic endovascular hypothermia was started almost 5 h after the event and maintained for 24 h (tympanic temperature at admission: 35.9-C). The CoolGard Icy Catheter (Alsius corp., Irvine, California, USA; 8,5 fr) was positioned in the right femoral vein. The patient’s core temperature was maintained between 32 and 34 C. An G. Zagli (&) S. Batacchi M. Bonizzoli A. Di Filippo A. Peris Intensive Care Unit, Emergency Department, Careggi Teaching Hospital, University of Florence, Viale Morgagni 85 6, 50134 Florence, Italy e-mail: giovanni.zagli@unifi.it

A 48-year-old woman with dyspnoea on exertion, anemia and thrombocytopenia

Dr. Micheli: A 48-year-old woman was admitted to our hospital after a 2-month history of dyspnoea on exertion. She did not report fever, sweats, chills, chest pain or recent weight loss. Twenty years before she had undergone mitral commissurotomy for rheumatic mitral stenosis. One week before current admission, the patient was seen in the emergency department (ED) because of paroxysmal atrial fibrillation. Synchronized electrical cardioversion was performed with recover of sinus rhythm. Echocardiography showed mitral stenosis with a valve area 1 cm and mild pulmonary hypertension. Results of routine laboratory tests were normal except for anemia and thrombocytopenia (platelet count 35,000/mm, hemoglobin 11.1 g/dl). Seven months before admission, these values were in the normal range. After discharge, the patient continued to experience dyspnoea while walking for a short distance and orthopnea. Eleven years before she had undergone excision of a right breast carcinoma, and had received a 6-month cycle of adjuvant chemotherapy. No local or systemic relapse had subsequently been documented. She worked as a pianist. There was no history of allergies. She did not report diabetes mellitus, illicit drug use, smoke history, alcohol use, hypertension, dyslipidemia or family history of heart disease or cancer. She did not consume medications except propafenone that had been prescribed in the ED a few days before. On physical examination, the patient was not in acute distress. Blood pressure was 115/70 mmHg, pulse rate 98 beats/min, respiratory rate16 breaths/min, temperature 36 C and SpO2 98% while she was breathing room air. Lungs fields were clear on auscultation. A low-frequency holodiastolic murmur and mitral valve opening snap were heard over the cardiac apex. There was neither peripheral oedema nor increased jugular venous pressure. Peripheral pulses were normal and symmetrical. Abdomen was soft and non-tender. No masses or enlarged organs were detectable. There were no petechiae, ecchymoses, skin rash or lymphadenopathy. Neurologic examination was unremarkable. An electrocardiogram showed sinus rhythm. A blood gas analysis was normal. Thrombocytopenia (38,000/mm) was confirmed and pseudo-thrombocytopenia was excluded. On second hospital day, the patient abruptly developed left hemiplegia and dizziness. A CT scan of the head excluded acute intracranial hemorrhage. NIHSS was 12. The hospital Stroke Team was alerted within 30 min after the onset of symptoms but thrombolytic therapy was not performed because of the low platelet count. The patient underwent cerebral angiography that revealed diffuse bilateral microemboli not suitable for mechanical revascularization. Transesophageal echocardiography showed left appendage thrombosis. Intravenous heparin therapy S. Del Pace C. Alderighi R. Rasoini (&) R. Alterini S. Micheli G. Santoro Clinica Medica Generale e Cardiologia, Department of Heart and Vessels, Azienda Ospedaliero-Universitaria Careggi, University of Florence, Viale Morgagni 85, 50134 Florence, Italy e-mail: raffaele.rasoini@tiscali.it

Partial safety of the new COX-2 inhibitor rofecoxib in NSAIDs high sensitive patients.

AllergyVolume 59, Issue 10 p. 1133-1134 Partial safety of the new COX-2 inhibitor rofecoxib in NSAIDs high sensitive patients A. Matucci, A. Matucci Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorP. Parronchi, P. Parronchi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorA. Vultaggio, A. Vultaggio Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorO. Rossi, O. Rossi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorF. Brugnolo, F. Brugnolo Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorE. Maggi, E. Maggi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorS. Romagnani, S. Romagnani Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this author A. Matucci, A. Matucci Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorP. Parronchi, P. Parronchi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorA. Vultaggio, A. Vultaggio Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorO. Rossi, O. Rossi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorF. Brugnolo, F. Brugnolo Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorE. Maggi, E. Maggi Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this authorS. Romagnani, S. Romagnani Department of Internal Medicine Section of Immunoallergology and Respiratory Diseases University of Florence Policlinico di Careggi Viale Morgagni 85 50134 Florence Italy Tel: +39 055 4296426 Fax: +39 055 412867 E-mail: [email protected]Search for more papers by this author First published: 07 September 2004 https://doi.org/10.1111/j.1398-9995.2004.00532.xCitations: 14 COX-2 inhibitor is relatively safe in patients with a high degree of NSAIDs hypersensitivity. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume59, Issue10October 2004Pages 1133-1134 RelatedInformation

Pharmacodynamic and pharmacokinetic considerations regarding new fluoroquinolones: [formula omitted] Department of Pharmacology, viale Morgagni, 65-50134 Firenze-ITALY

Pharmacodynamic and pharmacokinetic considerations regarding new fluoroquinolones: [formula omitted] Department of Pharmacology, viale Morgagni, 65-50134 Firenze-ITALY

Low-Dose Heparin Pretreatment is not Able to Prevent Clotting Activation during Coronary Angiography

The common use of coronary angiography in the treatment of coronary artery disease has 1. Methods prompted many investigations on changes in hemostasis activation during this procedure. Many 1.1. Patients factors may interfere with the results obtained: previous pharmacological treatments, catheterization The study population consisted of 25 consecutive, procedures, drugs administered during procedures, unselected patients with coronary artery disease (21 radiographic contrast media (CM), etc. [1]. An immen and 4 women), aged 41–73 years, referred to portant issue is the role played in hemostatic changes the Institute of Internal Medicine and Cardiology for by non ionic CM, which have been shown to be pocoronary angiography. All patients were on therapy tentially thrombogenic [2–4]. A limited number of with standard antianginal drugs. No patient had prein vivo studies have indicated that both platelet and existing hemostatic defects or anticoagulant treatclotting activation occur after coronary angiography ment. Aspirin (100–325 mg/day) had been taken performed by non ionic CM [3,5,6]. Recently, Mukfor at least one month before angiography by all herjee et al. [6] observed a marked blood clotting patients. The study was carried out according to activation during coronary angiography (not prethe principles of Helsinki declaration. ceded by heparin treatment), whereas such an activation was not found after PTCA in which a heparin bolus of 20000 IU was injected. No information is 1.2. Coronary Angiography available about the occurrence of blood clotting activation during coronary angiography performed by Coronary angiography was performed through the non ionic CM when a low dose of heparin is adminisfemoral approach with a 6 F catheter. All patients during the procedure received 3000 IU of heparin intravenously (i.v). About 150–200 ml of CM were Abbrevations: CM, constrast media; SPA, spontaneous platelet aggregation; TAT, thrombin-antithrombin complexes; PRP, plateinjected into coronary arteries during each examilet-rich-plasma. nation; the CM employed was a low-osmolar non Corresponding author: Rosanna Abbate, Clinica Medica Generale ionic one, iohexol sodium (Omnipaque-Nycomed, e Cardiologia, Universita di Firenze, Viale Morgagni 85, 50134 Firenze, Italia. Tel: 139 (55) 4277954; Fax: 139 (55) 4277608. Norway).

Wine complex phenols and tannins (CPT) protect against liver oxidative DNA damage induced by 2-nitropropane: [formula omitted], M. Lodovici, G. Paganelli and P. Dolara. Department of Pharmacology, University of Florence, Viale Morgagni 65, 50134, Florence Italy

Wine complex phenols and tannins (CPT) protect against liver oxidative DNA damage induced by 2-nitropropane: [formula omitted], M. Lodovici, G. Paganelli and P. Dolara. Department of Pharmacology, University of Florence, Viale Morgagni 65, 50134, Florence Italy

Source of IL‐4 able to induce the development of TH2‐like cells

Clinical & Experimental AllergyVolume 27, Issue 5 p. 488-500 Source of IL-4 able to induce the development of TH2-like cells M. RICCI, Corresponding Author M. RICCI Institute of Internal Medicine and Immunoallergology, University of Florence, ItalyProfessor M. Ricci. Istituto di Medicina Interna ed Immunoallergologia, Policlinico di Careggi. Viale Morgagni 85, 50134, Florence, Italy.Search for more papers by this authorA. MATUCCI, A. MATUCCI Division of Allergology and Clinical Immunology, Policlinico di Careggi-Florence, ItalySearch for more papers by this authorO. ROSSI, O. ROSSI Division of Allergology and Clinical Immunology, Policlinico di Careggi-Florence, ItalySearch for more papers by this author M. RICCI, Corresponding Author M. RICCI Institute of Internal Medicine and Immunoallergology, University of Florence, ItalyProfessor M. Ricci. Istituto di Medicina Interna ed Immunoallergologia, Policlinico di Careggi. Viale Morgagni 85, 50134, Florence, Italy.Search for more papers by this authorA. MATUCCI, A. MATUCCI Division of Allergology and Clinical Immunology, Policlinico di Careggi-Florence, ItalySearch for more papers by this authorO. ROSSI, O. ROSSI Division of Allergology and Clinical Immunology, Policlinico di Careggi-Florence, ItalySearch for more papers by this author First published: 27 April 2006 https://doi.org/10.1111/j.1365-2222.1997.tb00736.xCitations: 13AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume27, Issue5May 1997Pages 488-500 RelatedInformation

G-CSF for the prophylaxis of neutropenic fever in patients with small cell lung cancer receiving myelosuppressive antineoplastic chemotherapy: Meta-analysis and pharmaco-economic evaluation: Messori A, Trippoli S, Tendi E. Servizio Farmaceutico, DIC-CIF Policlinico di Careggi, viale Morgagni 85, 50134 Firenze. Clin Pharm Ther 1996;21:5743

G-CSF for the prophylaxis of neutropenic fever in patients with small cell lung cancer receiving myelosuppressive antineoplastic chemotherapy: Meta-analysis and pharmaco-economic evaluation: Messori A, Trippoli S, Tendi E. Servizio Farmaceutico, DIC-CIF Policlinico di Careggi, viale Morgagni 85, 50134 Firenze. Clin Pharm Ther 1996;21:5743

Regulation of fetal allograft survival by hormone-controlled Th1- and Th2-type cytokines : Piccinni M.-P., Romagnani S. Istituto di Medicina Interna, Immunoallergologia, Viale Morgagni 85, I-50134 Firenze, Italy [Immunologic Research 15(2), 141–150; 1996

Regulation of fetal allograft survival by hormone-controlled Th1- and Th2-type cytokines : Piccinni M.-P., Romagnani S. Istituto di Medicina Interna, Immunoallergologia, Viale Morgagni 85, I-50134 Firenze, Italy [Immunologic Research 15(2), 141–150; 1996

IL-4: a key cytokine in atopy.

Clinical & Experimental AllergyVolume 24, Issue 9 p. 801-812 IL-4: a key cytokine in atopy M RICCI, Corresponding Author M RICCI Istituto Clinica Medica III, University of Florence, Florence, ItalyProfessor M Ricci. Istituto di Clinica Medica III, Policlinico di Careggi. Viale Morgagni 85. 50134, Florence, Italy.Search for more papers by this author M RICCI, Corresponding Author M RICCI Istituto Clinica Medica III, University of Florence, Florence, ItalyProfessor M Ricci. Istituto di Clinica Medica III, Policlinico di Careggi. Viale Morgagni 85. 50134, Florence, Italy.Search for more papers by this author First published: September 1994 https://doi.org/10.1111/j.1365-2222.1994.tb01803.xCitations: 41AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume24, Issue9September 1994Pages 801-812 RelatedInformation

Platelet TxA2 receptors are reduced in IIa hyperlipo-proteinemia: [formula omitted], P.A. Modesti, I. Cecioni, R. Abbate, G.F. Gensini, G.G. Neri Serneri. Istituto di Clinica Medica I, University of Florence, Viale Morgagni, 85, Florence Italy

Platelet TxA2 receptors are reduced in IIa hyperlipo-proteinemia: [formula omitted], P.A. Modesti, I. Cecioni, R. Abbate, G.F. Gensini, G.G. Neri Serneri. Istituto di Clinica Medica I, University of Florence, Viale Morgagni, 85, Florence Italy

Free radical injury in skin cultured fibroblasts from Alzheimer's disease patients.

Oxygen radical production is postulated to be a major cause of cell damage in aging. We have studied the response to toxic oxygen metabolites of fibroblast cell lines derived from skin biopsies of patients with familial and sporadic Alzheimer's disease compared with those derived from normal controls. Fibroblasts were damaged by the generation of oxygen metabolites during the enzymatic oxidation of acetaldehyde by 50 mU of xanthine-oxidase. To quantify cell damage we measured lactate dehydrogenase activity in the culture medium and cell viability in fibroblast cultures from four normal subjects, five FAD, and four AD patients after 2 hours of Xo incubation. We found a significant increase of LDH activity in FAD vs. controls and also in AD vs. controls, suggesting that AD cells are more susceptible to oxygen radical damage than are normal controls.