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Antonia Pierobon,1 Elisa Sini Bottelli,1 Laura Ranzini,1 Claudio Bruschi,2 Roberto Maestri,3 Giorgio Bertolotti,4 Marinella Sommaruga,5 Valeria Torlaschi,1 Simona Callegari,1 Anna Giardini1 1Psychology Unit, 2Department of Pulmonary Rehabilitation, 3Department of Biomedical Engineering, Istituti Clinici Scientifici Maugeri, IRCCS, Montescano, 4Psychology Unit, Istituti Clinici Scientifici Maugeri, IRCCS, Tratate, 5Clinical Psychology and Social Support Unit, Istituti Clinici Scientifici Maugeri, IRCCS, Camaldoli, Italy Abstract: In addition to clinical comorbidities, psychological and neuropsychological problems are frequent in COPD and may affect pulmonary rehabilitation delivery and outcome. The aims of the study were to describe a COPD population in a rehabilitative setting as regards the patients depressive symptoms, anxiety, mild cognitive impairment (MCI) and self-reported adherence and to analyze their relationships; to compare the COPD sample MCI scores with normative data; and to investigate which factors might predict adherence to prescribed physical exercise. This was a multicenter observational cross-sectional study. Of the 117 eligible stable COPD inpatients, 84 were enrolled according to Global initiative for chronic Obstructive Lung Disease (GOLD) criteria (mainly in Stage III–IV). The assessment included Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), anxiety, depression and self-reported pharmacological and nonpharmacological adherence. From the MMSE, 3.6% of patients were found to be impaired, whereas from the MoCA 9.5% had a likely MCI. Patients referred had mild-severe depression (46.7%), anxiety (40.5%), good pharmacological adherence (80.3%) and difficulties in following prescribed diet (24.1%) and exercise (51.8%); they struggled with disease acceptance (30.9%) and disease limitations acceptance (28.6%). Most of them received good family (89%) or social (53%) support. Nonpharmacological adherence, depressi

Background: To evaluate the clinical outcome of patients with relapsed or refractory follicular lymphoma treated with immunochemotherapy, in vivo purging and high-dose therapy with autotransplant. Patients and methods: Sixty-four patients were enrolled in the trial. Primary end point was progression-free survival (PFS). Secondary end points were the in vivo purging effect on stem-cell harvest and the impact of molecular response on the outcome. Results: At enrollment, 59% of patients were PCR+ for bcl-2 rearrangement in bone marrow (PCR-informative). After the immunochemotherapy, before mobilization, 97% obtained complete response or partial response and 87% of patients informative for bcl-2 were molecularly negative. Sixty-one patients proceeded to in vivo purging and peripheral blood stem cell (PBSC) mobilization with rituximab and high-dose AraC. The median number of CD34+ cells collected was 16.6 × 106/kg. Of 33 PCR-informative patients, the harvests resulted in PCR- in all. Fifty-eight patients received high-dose therapy and autotransplant of in vivo purged PBSC. After a median follow-up of 3.5 years, 41 patients are in complete remission. Five-year PFS is 59%. Conclusion: This study demonstrates that patients with advanced relapsed or refractory follicular lymphoma treated with immunochemotherapy, in vivo purging and autotransplant may obtain long-lasting PFS. In bcl-2-positive patients, in vivo purging allows the harvest of lymphoma-free PBSC. Absence of the bcl-2 rearrangement after autotransplant is associated with persistent clinical remission.

[Background] To report on long-term results of a phase 3 trial comparing three versus five cycles of adjuvant chemotherapy (CT) with full-dose epirubicin+ifosfamide in high-risk soft tissue sarcomas (STS)., [Methods] Patients (pts) were randomized to receive three preoperative cycles of epirubicin 120 mg/m2 and ifosfamide 9 g/m2 (Arm A) or to receive the same three preoperative cycles plus two postoperative cycles (Arm B). Radiotherapy could be either delivered in the preoperative or in the postoperative setting. Non-inferiority of the primary end point, OS, was assessed by the confidence interval of the hazard ratio (HR; Arm A/Arm B) derived from Cox model., [Results] Between January 2002 and April 2007, 164 pts were assigned to arm A and 164 to arm B. At a median follow-up (FU) of 117 months (IQ range 103–135 months), 123 deaths were recorded: 58 in Arm A and 65 in Arm B. Ten-year OS was 61% for the entire group of patients: 64% in Arm A and 59% in Arm B. The intention-to-treat analysis confirmed that three cycles were not inferior to five cycles (one-sided 95% upper confidence limit was 1.24). A per protocol analysis was consistent with these results. Pts with leiomyosarcoma and undifferentiated pleomorphic sarcoma (UPS) had the lowest, and the highest response rates, respectively. Consistently, Leiomyosarcoma and UPS had the worse and the best prognosis, respectively., [Conclusions] At a longer FU, the non-inferiority of three cycles of a full-dose conventional CT in comparison to five is confirmed. Response to therapy is also confirmed to be associated with better survival. This regimen is currently tested within an ongoing international trial against three cycles of a neoadjuvant histology-tailored CT (ClinicalTrials.gov Identifier: NCT01710176).

Between December 1985 and February 1995, 260 orthotopic liver transplantations (OLTX) were performed on 238 patients at Niguarda Hospital. Sixty-three patients had hepatocellular carcinoma (HCC); in 13 of the patients HCC was incidental. All patients had negative lymph nodes. According to the Child classification, 13 patients were Child A, 30 Child B, and 18 Child C. According to the TNM classification, 11 patients were stage I, 22 stage II, 15 stage III, and 15 stage IVa. Pre-OLTX chemoembolization was performed on 25 patients. The perioperative mortality rate was 27% (17 patients). Overall survival and disease-free actuarial survival rates at 1, 3, and 5 years were 94%, 76%, 76%, and 83%, 75%, 75%, respectively. Survival curves were compared for 16 different variables. No difference was observed for all parameters analyzed except tumor site, TNM stage, pre-OLTX AFP levels and vascular infiltration. These results seem to demonstrate that the OLTX for unresectable HCC can be considered in specifically selected cases as the treatment of choice. An adequate tumor staging is also necessary for a better patient selection in order to increase survival

We performed a multicenter study to validate the concept that a simple comprehensive geriatric assessment (CGA) can identify elderly, non-fit patients with diffuse large B-cell lymphoma (DLBCL) in whom curative treatment is not better then palliation, and to analyze potential benefits of treatment modulation after further subdividing the non-fit category by CGA criteria. One hundred and seventy-three patients aged > 69 treated with curative or palliative intent by clinical judgement only were grouped according to CGA into fit (46%), unfit (16%) and frail (38%) categories. Two-year overall survival (OS) was significantly better in fit than in non-fit patients (84% vs. 47%; p < 0.0001). Survival in unfit and frail patients was not significantly different. Curative treatment slightly improved 2-year OS in unfit (75% vs. 45%) but not in frail patients (44% vs. 39%). CGA was confirmed as very efficient in identifying elderly patients with DLBCL who can benefit from a curative approach. Further efforts are needed to better tailor therapies in non-fit patients.

The hyperpolarization-activated I(h) current, coded for by hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels, controls synaptic integration and intrinsic excitability in many brain areas. Because of their role in pacemaker function, defective HCN channels are natural candidates for contributing to epileptogenesis. Indeed, I(h) is pathologically altered after experimentally induced seizures, and several independent data indicate a link between dysfunctional HCN channels and different forms of epilepsy. However, direct evidence for functional changes of defective HCN channels correlating with the disease in human patients is still elusive. By screening families with epilepsy for mutations in Hcn1 and Hcn2 genes, we found a recessive loss-of-function point mutation in the gene coding for the HCN2 channel in a patient with sporadic idiopathic generalized epilepsy. Of 17 screened members of the same family, the proband was the only one affected and homozygous for the mutation. The mutation (E515K) is located in the C-linker, a region known to affect channel gating. Functional analysis revealed that homomeric mutant, but not heteromeric wild-type/mutant channels, have a strongly inhibited function caused by a large negative shift of activation range and slowed activation kinetics, effectively abolishing the HCN2 contribution to activity. After transfection into acutely isolated newborn rat cortical neurons, homomeric mutant, but not heteromeric wild type/mutant channels, lowered the threshold of action potential firing and strongly increased cell excitability and firing frequency when compared with wild-type channels. This is the first evidence in humans for a single-point, homozygous loss-of-function mutation in HCN2 potentially associated with generalized epilepsy with recessive inheritance.

The Brugada syndrome (BS) is a genetically transmitted arrhythmogenic disease, which requires risk stratification, especially in asymptomatic subjects. Recent studies have shown that magnetocardiographic mapping (MCG) at rest can detect abnormal current distribution located in the RVOT. Here we describe an asymptomatic 28 years old BS patient, studied with 12-lead ECG and 36-channel MCG for three times at rest, under effort and during flecainide (Flec) tests, along a four years follow-up. He had a type 2 BS ECG at rest, but normal physical examination, echocardiogram and MRI. Molecular screening of the SCNC5A open reading frame revealed a de novo missense mutation in the DII DIII linker, confirming the diagnosis of BS. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) dynamics and MF gradient orientation, were computed during the ST interval and at the T wave peak. Current density reconstruction (CDR) and the strength of the equivalent current dipole (ECD) were calculated during the JT interval, to evidence potentially arrhythmogenic current flowing. In spite of Flec-induced ECG abnormality (typical type-1 ST elevation in V1 V3), MCG didn't show clear-cut variation of VR parameters, which didn't differ from those of healthy controls, at rest and under effort. After Flec, CDR, calculated every 10 ms from the J point, evidenced a change in the direction of the strongest current toward the right ventricular outflow tract, without a significant increase of the JT ECD strength. During the follow-up the patient was asymptomatic and no arrhythmia occurred. Further work is deserved to establish the predictive value of MCG for non-invasive risk stratification in asymptomatic BS patients with abnormal Flec test.

The Brugada syndrome (BS) is a genetically transmitted arrhythmogenic disease, which requires risk stratification, especially in asymptomatic subjects. Recent studies have shown that magnetocardiographic mapping (MCG) at rest can detect abnormal current distribution located in the RVOT. Here we describe an asymptomatic 28 years old BS patient, studied with 12-lead ECG and 36-channel MCG for three times at rest, under effort and during flecainide (Flec) tests, along a four years follow-up. He had a type 2 BS ECG at rest, but normal physical examination, echocardiogram and MRI. Molecular screening of the SCNC5A open reading frame revealed a de novo missense mutation in the DII DIII linker, confirming the diagnosis of BS. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) dynamics and MF gradient orientation, were computed during the ST interval and at the T wave peak. Current density reconstruction (CDR) and the strength of the equivalent current dipole (ECD) were calculated during the JT interval, to evidence potentially arrhythmogenic current flowing. In spite of Flec-induced ECG abnormality (typical type-1 ST elevation in V1 V3), MCG didn't show clear-cut variation of VR parameters, which didn't differ from those of healthy controls, at rest and under effort. After Flec, CDR, calculated every 10 ms from the J point, evidenced a change in the direction of the strongest current toward the right ventricular outflow tract, without a significant increase of the JT ECD strength. During the follow-up the patient was asymptomatic and no arrhythmia occurred. Further work is deserved to establish the predictive value of MCG for non-invasive risk stratification in asymptomatic BS patients with abnormal Flec test.

The Brugada syndrome (BS) is a genetically transmitted arrhythmogenic disease, which requires risk stratification, especially in asymptomatic subjects. Recent studies have shown that magnetocardiographic mapping (MCG) at rest can detect abnormal current distribution located in the RVOT. Here we describe an asymptomatic 28 years old BS patient, studied with 12-lead ECG and 36-channel MCG for three times at rest, under effort and during flecainide (Flec) tests, along a four years follow-up. He had a type 2 BS ECG at rest, but normal physical examination, echocardiogram and MRI. Molecular screening of the SCNC5A open reading frame revealed a de novo missense mutation in the DII DIII linker, confirming the diagnosis of BS. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) dynamics and MF gradient orientation, were computed during the ST interval and at the T wave peak. Current density reconstruction (CDR) and the strength of the equivalent current dipole (ECD) were calculated during the JT interval, to evidence potentially arrhythmogenic current flowing. In spite of Flec-induced ECG abnormality (typical type-1 ST elevation in V1 V3), MCG didn't show clear-cut variation of VR parameters, which didn't differ from those of healthy controls, at rest and under effort. After Flec, CDR, calculated every 10 ms from the J point, evidenced a change in the direction of the strongest current toward the right ventricular outflow tract, without a significant increase of the JT ECD strength. During the follow-up the patient was asymptomatic and no arrhythmia occurred. Further work is deserved to establish the predictive value of MCG for non-invasive risk stratification in asymptomatic BS patients with abnormal Flec test.

The Brugada syndrome (BS) is a genetically transmitted arrhythmogenic disease, which requires risk stratification, especially in asymptomatic subjects. Recent studies have shown that magnetocardiographic mapping (MCG) at rest can detect abnormal current distribution located in the RVOT. Here we describe an asymptomatic 28 years old BS patient, studied with 12-lead ECG and 36-channel MCG for three times at rest, under effort and during flecainide (Flec) tests, along a four years follow-up. He had a type 2 BS ECG at rest, but normal physical examination, echocardiogram and MRI. Molecular screening of the SCNC5A open reading frame revealed a de novo missense mutation in the DII-DIII linker, confirming the diagnosis of BS. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) dynamics and MF gradient orientation, were computed during the ST interval and at the T wave peak. Current density reconstruction (CDR) and the strength of the equivalent current dipole (ECD) were calculated during the JT interval, to evidence potentially arrhythmogenic current flowing. In spite of Flec-induced ECG abnormality (typical type-1 ST elevation in V1-V3), MCG didn't show clear-cut variation of VR parameters, which didn't differ from those of healthy controls, at rest and under effort. After Flec, CDR, calculated every 10 ms from the J point, evidenced a change in the direction of the strongest current toward the right ventricular outflow tract, without a significant increase of the JT ECD strength. During the follow-up the patient was asymptomatic and no arrhythmia occurred. Further work is deserved to establish the predictive value of MCG for non-invasive risk stratification in asymptomatic BS patients with abnormal Flec test. © 2007.

Body surface potential mapping studies suggest that the induction rate of VT in Brugada syndrome (BrS) correlates with the area of ST elevation and the presence of late potentials, but also that ST elevation might be primarily caused by abnormality in depolarization rather than in repolarization, especially in the right ventricle outflow tract (RVOT). A preliminary study with magnetocardiographic (MCG) mapping at rest has shown an abnormal current distribution located in the RVOT. In this study we describe MCG patterns at rest, during physical effort and during flecainide test in an asymptomatic patient with BrS, restudied three times during three years follow-up. Method: An asymptomatic 28 years old man, with a type 2 BrS ECG at rest, but normal physical examination, echocardiogram and MRI, was studied with 12-lead ECG and multichannel MCG mapping, recorded with a 36-channel DC-SQUID system (CMI-2436), (sensitivity 20 fT/Hz1⁄2), at rest, during effort and flecainide tests. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) gradient orientation (a angle) was computed at the integral of the second quarter of the ST interval and at the T-wave apex. Current density imaging (CDI) and the strength (in mAm) of the equivalent current dipole (ECD) were calculated during all the first and second quarter of the J-T interval, to estimate potentially arrhythmogenic current flowing. Results: Molecular screening of the SCNC 5A open reading frame revealed a de novo missense mutation in the DII-DIII linker, thus confirming the diagnosis of BrS. Flecainide induced typical type-1 ST elevation in V1-V3 leads, but no changes of MF a angles, which were normal at rest and under effort. After flecainide, CDI evidenced a shift of the current density at the J-point, from right to left epicardial surface, without a significant increase of the J-T ECD strength. Conclusions: In this asymptomatic BrS patient, in spite of positive flecainide at the ECG, MCG mapping didn’t

Recent body surface potential mapping studies suggest that the induction rate of VT in Brugada syndrome (BrS) correlates with the area of ST elevation and the presence of late potentials, but also that ST elevation might be primarily caused by abnormality in depolarization rather than in repolarization, especially in the right ventricle outflow tract (RVOT). A preliminary study with magnetocardiographic (MCG) mapping at rest has shown an abnormal current distribution located in the RVOT. In this study we describe MCG patterns at rest, during physical effort and during flecainide test in an asymptomatic patient with BrS, restudied three times during three years follow-up. Method: An asymptomatic 28 years old man, with a type 2 BrS ECG at rest, but normal physical examination, echocardiogram and MRI, was studied with 12-lead ECG and multichannel MCG mapping, recorded with a 36-channel DC-SQUID system (CMI-2436), (sensitivity 20 fT/Hz1⁄2), at rest, during effort and flecainide tests. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) gradient orientation (a angle) was computed at the integral of the second quarter of the ST interval and at the T-wave apex. Current density imaging (CDI) and the strength (in mAm) of the equivalent current dipole (ECD) were calculated during all the first and second quarter of the J-T interval, to estimate potentially arrhythmogenic current flowing. Results: Molecular screening of the SCNC 5A open reading frame revealed a de novo missense mutation in the DII-DIII linker, thus confirming the diagnosis of BrS. Flecainide induced typical type-1 ST elevation in V1-V3 leads, but no changes of MF a angles, which were normal at rest and under effort. After flecainide, CDI evidenced a shift of the current density at the J-point, from right to left epicardial surface, without a significant increase of the J-T ECD strength. Conclusions: In this asymptomatic BrS patient, in spite of positive flecainide at the ECG, MCG mapping

Between January 1989 and June 1997, 533 patients (423 male, 110 female, mean age 61 years, range 22-89 years) with hepatocellular carcinoma (HCC) were observed at our center. We report on 419 patients retrospectively compared for different treatments: liver transplantation (LT; 55 patients), resective surgery (RS; 41 patients), transarterial chemoembolization (TACE; 171 patients) and percutaneous ethanol injection (PEI; 152 patients). The 3- and 5-year actuarial survival rates were, respectively, 72% and 68% for LT, 64 and 44% for RS, 54 and 36% for PEI, and 32 and 22% for TACE. Survival curves were compared for sex, age, tumor characteristics, alphafetoprotein level, Child class, and etiology of cirrhosis. All patient-related characteristics examined (sex, age) are not significantly related to patient survival. Tumor-related variables and associated liver disease variables significantly conditioned survival in relation to different treatments. LT seems to be the treatment of choice for monofocal HCC less then 5 cm in diameter and in selected cases of plurifocal HCC. © Springer-Verlag 1998

An unclassified amicrobial pustular dermatosis particularly affecting the main cutaneous folds, external auditory canals and scalp and coexisting with systemic lupus erythematosus has been recently described.

Anglés y Subirá, Eitner, R. Biographish-bibliographisches Quellen Lexikon der Musiker und Musikgelehrten christlicher Zeitrechnung bis Mitte des neunzehnten Jahrhunderts, 1959, Sign.: A-M⁴, N-Z⁸, 2A-2B⁸, 2C⁶, 2E⁸, 2D⁶, Iniciales xilográficas

Anglés y Subirá, Eitner, R. Biographish-bibliographisches Quellen Lexikon der Musiker und Musikgelehrten christlicher Zeitrechnung bis Mitte des neunzehnten Jahrhunderts, 1959, Sign.: A-M⁴, N-Z⁸, 2A-2B⁸, 2C⁶, 2E⁸, 2D⁶, Iniciales xilográficas