Experience measuring antibodies to both drug and impurities and their clinical sequelae.
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Antibodies↗
Biomedical subjects
P Gallo
Publications and source records attributed to P Gallo.
Indirect ELISA for the diagnosis of brucellosis in water buffaloes (Bubalus bubalis) in Italy.
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Animals↗
The HLA-DR13 haplotype is associated with "benign" multiple sclerosis in northeast Italy.
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Adult↗
Cerebrospinal fluid examination in the differential diagnosis of inflammatory myelopathies.
Among the diagnostic procedures aimed at defining the etiology and the pathogenesis of inflammatory myelopathies, the examination of the cerebrospinal fluid (CSF) plays a central role. Indeed, for several autoimmune and inflammatory syndromes and diseases involving the spinal cord, in addition to immunological screening of the blood, a detailed analysis of the CSF may allow the achievement of the diagnosis. Routine CSF analysis should include a detailed cytology, the evaluation of the blood-brain barrier dysfunction, quantitative and qualitative analysis of the intrathecal IgG synthesis (i.e. calculation of the IgG index and demonstration of oligoclonal IgG bands), and immunological and virological tests based on immunoenzymatic (ELISA, RIA) and molecular biology techniques (PCR, nested PCR). A more advanced step includes fluorescence-activated cell sorting (FACS) analysis of CSF lymphocytes, and, when possible, virological and immunological tests on cell culture supernatants.
Autoimmune Diseases↗
Arrhythmogenic right ventricular cardiomyopathy: clinicopathologic correlation based on a revised definition of pathologic patterns.
Different morphologic features of arrhythmogenic right ventricular cardiomyopathy (ARVC) have been described. However, it is still unclear whether they correspond to distinct forms of the same disease. A pathologic study was performed on a series of ARVC (15 from heart transplant and 12 from autopsy) from 2 Italian referral university hospitals. Based on both myocellular features and the nature of myocardial replacement, hearts were divided into 2 groups: infiltrative, with a lacelike pattern of transmural fatty infiltration and strands of normal residual cardiomyocytes (n = 11); and cardiomyopathic, with massive myocardial replacement by fibro fatty tissue and cardiomyopathic changes (such as hypertrophy and myofibril loss) of residual cardiomyocytes (n = 16). Hearts from the infiltrative group were mostly obtained at autopsy of patients who died suddenly. Fatty substitution was limited almost exclusively to the right ventricle. Mitral valve dysplasia (prolapse or cleft) was frequently present. Hearts from the cardiomyopathic group came mainly from heart transplants for congestive heart failure. Fibro fatty replacement was more extensive, usually biventricular. Active myocarditis and features suggestive of myocardial transdifferentiation were also observed. Despite these differences in clinical outcome and morphologic features, patients from the 2 groups showed similar mean age, sex distribution, occurrence of threatening ventricular arrhythmias, and prevalence of family history of sudden death, arrhythmias, or cardiomyopathy. Infiltrative and cardiomyopathic patterns represent different clinical and pathologic subsets of ARVC. Myocellular features are an important clue in the distinction between the two entities. The differentiation between the 2 patterns is feasible on endomyocardial biopsy and could give important prognostic information.
Adipose Tissue↗
Pathological findings of HIV-associated cardiovascular disease.
More effective therapies have improved survival times of HIV+ patients, resulting in a higher prevalence of long-term complications of the disease. This review focuses on HIV-associated cardiovascular pathology, correlating the morphologic findings to clinical syndromes of HIV disease/AIDS.
Cardiomyopathies↗
The range of multiple sclerosis associated with neurofibromatosis type 1.
Multiple sclerosis associated with neurofibromatosis type 1 (NF1) is a very rare event. Seven patients with multiple sclerosis and NF1 are described in the literature, and all were reported to have the primary progressive form of multiple sclerosis. Three new patients with NF1 that developed multiple sclerosis are described and it is shown that the range of multiple sclerosis associated with NF1 includes the relapsing forms of the disease. The risk of having both NF1 and multiple sclerosis in north east Italy is higher than would be expected based on the prevalence rates of the two diseases.
Adult↗
Home palliative care as a cost-saving alternative: evidence from Catalonia.
The aim of this study was to provide a comparative assessment of the health care resources consumed during the final month of life of patients undergoing palliative treatment and who died from cancer in the town of Mataró, Spain, in 1998, with respect to whether they benefited from home care teams or not. Relevant differences in the use of health care resources were found between the groups. Patients in the standard care group presented more hospital care admissions and longer length of stay, higher use of emergency and outpatient visits, and greater use of palliative care units within nursing homes than patients in the home care group. The monetary quantification of the use of the above-mentioned resources showed a 71% increase in the cost per patient in the standard care when compared to home care. According to the results of this study, home care teams for terminal cancer patients allow for savings to the health care system. A series of policy making and health services research implications are discussed.
Aged↗
Increased expression of thyroid hormone receptor isoforms in end-stage human congestive heart failure.
Thyroid hormone plays an important role on myocardial development and function. The local effects of thyroid hormone are mediated by the receptor isoforms ultimately driving the expression of cardiac-specific genes. Although overt and subclinical thyroid dysfunction causes well-known changes in the cardiovascular system, little is known about local thyroid hormone action in normal and failing human myocardium. With a newly developed multiplex competitive RT-PCR method, we evaluated the expression of thyroid hormone receptor (TR) isoforms alpha-1, alpha-2, and beta-1 in normal human hearts and in end-stage congestive heart failure. A statistically significant difference in the expression of all three TR isoforms was observed among samples from normal subjects, ischemic heart disease (IHD), and dilated cardiomyopathy (DCM). In DCM, compared with normal, the studied TR isoforms were significantly increased. In IHD, the increased expression was found significant only for alpha-1 and alpha-2 isoforms. No differences were observed between the pathologic groups. In conclusion, a coordinated increment in the expression of the TR isoforms was observed in both DCM and IHD by multiplex competitive RT-PCR. The observed changes could represent a compensatory mechanism to myocardial failure or to locally altered thyroid hormone action.
Adult↗
Hemorrhage in cerebral metastasis from angiosarcoma of the heart: case report.
The purpose of this article is to describe the clinical and pathological features of metastatic angiosarcoma in the central nervous system. Only a few cases of cerebral metastasis from angiosarcoma of the heart have been recorded in the literature; particularly related to intracerebral hemorrhage. A case of secondary cerebral angiosarcoma of the heart in a 33 years old man is presented. The initial symptoms were headache, vomiting, lethargy and aphasia. There was a mass in the left temporal lobe with hemorrhage and edema on the computerized tomography (CT). After 24 hours the neurological status worsened and another CT scan showed rebleeding on the tumor area. He underwent an emergency craniotomy but died two days after. Considering the longer survival of sarcoma patients with new modalities of treatment, the incidence of brain metastasis may increase, demanding a better preventive and more aggressive approach. Besides, due to the hemorrhagic nature of such lesions, we suggest the immediate surgery to prevent a fast and lethal evolution because rebleeding.
Adult↗
Interferon-beta (INF-beta) antibodies in interferon-beta1a- and interferon-beta1b-treated multiple sclerosis patients. Prevalence, kinetics, cross-reactivity, and factors enhancing interferon-beta immunogenicity in vivo.
We analysed the role of dosage, route and frequency of administration of clinical grade interferon-beta (IFN-beta) preparations in inducing anti-IFN-beta antibodies (IFN-beta-Abs) in 5 groups of relapsing-remitting multiple sclerosis (RRMS) patients who were respectively treated as follows: 1) weekly intramuscular (i.m.) injections of 30 mg of recombinant IFN-beta1a (Avonex), 2) subcutis (s.c.) injections of 250 mg IFN-beta1b (Betaferon) every other day, 3) weekly i.m. injections of 250 mg IFN-beta1b (Betaferon), 4) s.c. injections of 22 mg of IFN-beta1a (Rebif) three times a week, and 5) i.m. injections of 22 mg of IFN-beta1a (Rebif) twice a week. IFN-beta-Abs were determined by ELISA. IFN-beta1b was more immunogenic than IFN-beta1a not only when administered s.c. every other day, but also when administered i.m. at a lower weekly dose; i.m. injection, however, significantly delayed the appearance, and induced lower serum levels of IFN-beta-Abs. In patients treated with s.c. IFN-beta1b, Ab levels peaked 3 to 9 months after therapy initiation, and then slowly, but progressively, declined to pre-therapy levels that in some patients were reached after three years. Patients treated with i.m. or s.c. IFN-beta1a only rarely developed IFN-beta-Abs, and then at very low titers. Overall, the i.m. weekly administration of IFN-beta1a was the less immunogenic treatment. In IFN-beta1b-treated patients, a wash-out period of two/three months was sufficient to bring the IFN-beta-Ab levels below the cut-off. Our findings suggest that the immunogenicity of IFN-beta1a is low, regardless of the route of administration and the dosage, while that of IFN-beta1b is high, and is significantly, but not completely reduced by i.m. administration. As IFN-beta-Abs are cross-reactive, a wash-out period is suggested when the preparation is changed from IFN-beta1b to IFN-beta1a in order to maintain the clinical benefits of the therapy.
Antibodies↗
Detection of Brucella species in buffalo whole blood by gene-specific PCR.
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Animals↗
Supercooled confined water and the mode coupling crossover temperature
We present a molecular dynamics study of the single-particle dynamics of supercooled water confined in a silica pore. Two dynamical regimes are found. Close to the hydrophilic substrate molecules are below the mode coupling crossover temperature, T(C), already at ambient temperature. The water closer to the center of the pore (free water) approaches upon supercooling T(C) as predicted by mode coupling theories. For free water the crossover temperature and crossover exponent gamma are extracted from power-law fits to both the diffusion coefficient and the relaxation time of the late alpha region.
Journal Article↗
Human parvovirus B19 infection in infancy associated with acute and chronic lymphocytic myocarditis and high cytokine levels: report of 3 cases and review.
Human parvovirus B19 infection is occasionally associated with acute lymphocytic myocarditis (ALM). Three infants with B19 virus-associated ALM were followed up clinically, histologically, and immunovirologically. Each infant had B19 virus DNA in the blood or B19 virus-specific IgM antibodies. Two infants with postnatal infection recovered after immunosuppressive therapy. The third infant with possible prenatal infection developed chronic persistent myocarditis associated with persistent B19 virus DNA in the blood. All 3 infants had increased levels of interferon-gamma, tumor necrosis factor-alpha, and interleukins -6 and -8. Four newborns with congenital B19 virus infection and 4 infants and children who had postnatally acquired B19 virus infection without myocarditis all had normal levels of these cytokines. These observations suggest that B19 virus infection in infancy causes ALM in some infants and children.
Acute Disease↗
Effect of IFNbeta and anti-IFNbeta antibodies on NK cells in multiple sclerosis patients.
We analysed longitudinally the numbers of CD3-CD16+ (natural killer cells, NK) and CD3-CD57+ cells (a subset of NK) in 15 IFNbeta1b- and 12 IFNbeta1a-treated relapsing-remitting multiple sclerosis (RRMS) patients. IFNbeta1b (Betaferon)-treated RRMS patients showed a rapid and marked reduction in the number of both NK subsets which started 1 month after therapy initiation, and reached highest significance after 3 months (P=0.000); however, figures reverted to pre-treatment values following the appearance of anti-IFNbeta antibodies. In IFNbeta1a (Avonex)-treated RRMS patients, the decrease in both CD3-CD16+ and CD3-CD57+ cell number was slower but more persistent; anti-IFNbeta antibodies were only rarely detected in these patients, and at lower titers than in IFNbeta1b-treated ones. Our findings suggest that NK cells might be one of the major immunological targets of IFNbeta-based treatments.
Adult↗
Class A helix-loop-helix proteins are positive regulators of several cyclin-dependent kinase inhibitors' promoter activity and negatively affect cell growth.
The class A of basic helix-loop-helix (bHLH) proteins are ubiquitously expressed transcription factors playing a pivotal role in the regulation of cell growth and differentiation. We determined that enforced expression of all four different mammalian members of this family, E12, E47, E2-2, and HEB, suppresses the cell colony-forming efficiency of several cell lines. To gain insights into the mechanisms by which class A bHLH factors affect cell growth, we have investigated their role in the transcriptional regulation of cyclin-dependent kinase inhibitors. We found that p21CIP1/ WAF1, p15INK4B, and p16INK4B promoter sequences contain E-boxes that render these genes competent for class A bHLH-mediated transcriptional activation and Id-mediated repression. The mechanism underlying the class A bHLH-mediated inhibition of cell growth does not involve an arrest of G1 progression in 293T cells. In fact, contrary to what has been found in 3T3 NIH fibroblasts, we found that enhanced expression of class A bHLH proteins led to a decreased proliferation rate by promoting cell death associated with the induction of apoptosis. These findings highlight the role of the class A bHLH proteins as general negative regulators of cell proliferation through a mechanism(s) that involves both enhancement of several cyclin-dependent kinase inhibitor genes expression and promotion of cell death.
Animals↗
Differential role for Sp1/Sp3 transcription factors in the regulation of the promoter activity of multiple cyclin-dependent kinase inhibitor genes.
Cyclin-dependent kinase inhibitors play a significant role in cell cycle progression and in cellular differentiation and their expression is regulated in different cellular settings. GC-rich regions in the promoter sequences of the cyclin-dependent kinase inhibitor genes p15INK4B and p21CIP1/WAF1 mediate the transcriptional response of these genes to extracellular stimuli. Similar GC-rich sequences in the promoter of the p15INK4A and p16INK4B gene can be targeted for transcriptional inactivation by methylation of cytosine residues. GC-rich regions represent putative target sites for binding of the ubiquitously expressed Sp1 and Sp3 transcription factors. Using a combination of functional and biochemical studies, we analyzed the potential role of the Sp1 and Sp3 factors in the regulation of CDKI p15, p16, and p21 promoter activities. Using transient reporter gene assays, we determined that Sp1 is a strong activator of these promoters, whereas Sp3 functions as a weak transactivator. We have identified multiple protein-binding sites in the proximal promoter sequences of these genes by footprinting analysis. Some of these sites are bound by Sp1 and Sp3, as demonstrated by gel-shift experiments using Sp1/Sp3-specific antibodies, permitting the demonstration that a differential role exists for Sp1 and Sp3 in the regulation of the activity of these promoters.
Animals↗
Valsartan in acute myocardial infarction trial (VALIANT): rationale and design.
BACKGROUND: Survivors of acute myocardial infarction (MI) complicated by heart failure and/or resulting in left ventricular dysfunction are at heightened risk for subsequent death and major nonfatal cardiovascular events. Inhibition of the renin-angiotensin system with an angiotensin-converting enzyme inhibitor has consistently been demonstrated to result in reductions in these risks by approximately 20%. The development of angiotensin II receptor blockers offers a new, more specific, and theoretically more complete pharmacologic mode to inhibit the adverse influence of angiotensin II. METHODS: Valsartan in Acute Myocardial Infarction (VALIANT) is a multicenter, double-blind, randomized, active controlled parallel group study comparing the efficacy and safety of long-term treatment with valsartan, captopril, and their combination in high-risk patients after MI. The trial is designed with 3 arms, giving equal statistical consideration to survival comparisons of captopril versus the angiotensin II receptor blocker valsartan, as well as the combination of captopril plus valsartan, compared with a proven effective dose of captopril. This 14,500-patient trial is designed with an 86% power to detect a 15% reduction in mortality rate with either use of valsartan compared with captopril. The trial encourages optimal individualization of other proven therapies in acute and chronic infarction, and the international patient body ensures good representation of multiple practice patterns. CONCLUSION: VALIANT is a large international investigative effort that will evaluate the role of valsartan in the management of patients with MI associated with heart failure and/or left ventricular dysfunction. The use of a proven dose of captopril and the comparator arms with valsartan alone or in combination with captopril provides a unique test of whether the angiotensin II receptor blocker can make an additional improvement in clinical outcomes beyond angiotensin-converting enzyme inhibitors.
Angiotensin II↗