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Biomedical subjects

D Galimberti

Publications and source records attributed to D Galimberti.

At least 19 recordsLinked to original sources
PubMed2006

The leukocyte expression of CD36 is low in patients with Alzheimer's disease and mild cognitive impairment.

CD36, a scavenger receptor of class B (SR-B), helps mediate microglial and macrophage response to beta-amyloid fibrils (betaA), and seems to play a key role in the proinflammatory events associated with Alzheimer disease (AD) in many tissues. Peripheral leukocytes express many molecules and multiple receptors which undergo the same regulatory mechanisms as those operative in the brain. Thus, these cells, easily obtainable through peripheral blood sampling, may be used as a tool to investigate changes occurring in inaccessible brain areas. Based on these premises, we investigated the leukocyte expression of CD36 in 70 AD patients and in 30 subjects with mild cognitive impairment (MCI). Results were compared to those of 20 young and 40 age-matched control subjects. Leukocyte expression of CD36 was significantly reduced versus controls in both AD and MCI patients, while in young and old controls there were no age-related changes. Although preliminary, these data indicate that the reduction of CD36 expression in leukocytes is a disease-related phenomenon, occurring since the early stages of AD (MCI). Irrespective of the mechanism(s) underlying such changes, assessment of leukocyte CD36 expression might represent an useful tool to support the diagnosis of AD and to screen MCI patients candidates to develop the disease.

Adult↗
PubMed2006

Genetics and neurobiology of frontotemporal lobar degeneration.

Frontotemporal dementia (FTD) is characterised by brain intracellular deposition of abnormally phosphorylated tau protein, considered responsible for neuronal death. Several familial cases with different mutations in the tau encoding gene (MAPT), located on chromosome 17, have been described. Besides, in a Danish family, the genetic defect has been associated to chromosome 3. Although many FTD families exhibit known mutations, in some cases none of them occur. Recent findings demonstrate an increased intrathecal production of both pro- and anti-inflammatory cytokines in sporadic FTD patients. Besides, increased cerebrospinal fluid monocyte chemotactic protein-1 and interleukin-8 levels have been observed in FTD, whereas interferon-gamma-inducible protein-10 levels were similar to controls.

Dementia↗
PubMed2005

Efficacy and safety of topiramate in infants according to epilepsy syndromes.

Studies of the efficacy of topiramate (TPM) in infants and young children are few. Here we report an open, prospective, and pragmatic study of effectiveness of TPM in terms of epilepsy syndromes, in children aged less than 2 years. The median follow-up period was 11 months. We enrolled 59 children in the study: 22 affected by localization-related epilepsy (LRE), 23 by generalized epilepsy, six by Dravet's syndrome, and eight with unclassifiable epilepsy. TPM was effective (responders showed a decrease of more than 50% in seizure frequency) in 47% of patients, including 13% who were seizure-free at the last visit. TPM was more effective in localization-related epilepsy (48% of responders) than in generalized epilepsy (32% of responders). In the latter group, 19 patients suffered from infantile spasms. Four of six patients with cryptogenic infantile spasms became seizure-free. Of the 13 patients with symptomatic infantile spasms, only one was seizure-free. Results were poor for patients with Dravet's syndrome. In general, TPM was well tolerated. The most frequently reported adverse effects were drowsiness, irritability, hyperthermia, and anorexia. The present study concludes that TPM is effective for a broad range of seizures in infants and young children and represents a valid therapeutic option in this population.

Anorexia↗
PubMed2005

Rubella and measles seroprevalence among women of childbearing age, Argentina, 2002.

To assess rubella and measles susceptibility among women of childbearing age we conducted a cross-sectional seroprevalence study in four cities and one rural area in Argentina. A convenience sample of women aged 15-49 years seeking care in public health-care institutions was selected (n=2804). Serum specimens were tested for rubella and measles IgG antibody titres. The overall susceptibility to rubella and measles was 8.8 and 12.5% respectively. Seroprevalence differences were found for both rubella (P<0.001) and measles (P=0.002) across sites. Rubella seroprevalence was higher in women aged >or=40 years than in younger women (P=0.04). Measles seroprevalence tended to increase with age (P<0.001). Approximately 15% of women aged 15-29 years were not immune to measles. No risk factors were associated with rubella seronegativity; however, age (P<0.001) and having less than four pregnancies (P<0.001) were factors associated with measles seronegativity. Our findings support the introduction of supplemental immunization activities targeting adolescents and young adults to prevent congenital rubella syndrome and measles outbreaks over time.

Adolescent↗
PubMed2004

Serum levels of chitotriosidase as a marker of disease activity and clinical stage in sarcoidosis.

BACKGROUND: Sarcoidosis is a systemic granulomatous disease characterized by T-lymphocyte activation and lymphocyte migration into involved organs, usually the lungs. The amounts of a number of biochemical markers, such as angiotensin converting enzyme (ACE) activity, increase in the serum of patients with sarcoidosis. Chitotriosidase is an enzyme secreted by activated macrophages able to catalyze the hydrolysis of both chitin and chitin-like substrates. Chitotriosidase is involved in defense against, and in degradation of chitin-containing pathogens such as fungi, nematodes, and insects. METHODS: Forty-three patients affected by chronic sarcoidosis, in active (23 patients) or inactive (20 patients) phase, were studied. Serum levels of chitotriosidase and ACE activity were evaluated and compared with those of 32 healthy subjects. Serum chitotriosidase concentration and ACE activity were also correlated with radiographic stage of disease. RESULTS: Individuals with chronic sarcoidosis have higher serum chitotriosidase concentrations and ACE activity than those of normal subjects. Sarcoidosis patients in the active phase of the disease had significantly higher chitotriosidase and ACE levels than those in the inactive phase. In contrast to serum ACE activity, a significant relationship between serum levels of chitotriosidase and the four radiographic stages of the disease was observed. CONCLUSION: Although the data need to be validated by further investigation, the observations made in this study seem to indicate that serum chitotriosidase concentrations may be a useful marker for monitoring sarcoidosis disease activity and prognosis.

Acute Disease↗
PubMed2002

Plasma ghrelin concentrations in elderly subjects: comparison with anorexic and obese patients.

Ghrelin, a novel endogenous ligand for the GH secretagogue receptor, has been reported to stimulate GH secretion and food intake in both humans and other animals. Interestingly, recent data indicate that ghrelin is up- and down-regulated in anorexia nervosa (AN) and obesity, which are also known to be accompanied by increased and reduced GH levels respectively. Ageing is associated with a gradual but progressive reduction in GH secretion, and by alterations in appetite and food intake. The role of ghrelin in the decline of somatotroph function and the anorexia of ageing is unknown. To investigate the influence of age on circulating levels of ghrelin, a total of 19 young and old normal weight subjects (Y-NW, n=12; O-NW, n=7), six patients with active AN (A-AN), and seven patients with morbid obesity (OB) were studied. In addition to fasting plasma ghrelin concentrations, baseline serum TSH, IGF-I and insulin levels were measured. Mean plasma ghrelin concentrations in A-AN or OB were higher and lower respectively than those present in Y-NW. Interestingly, mean plasma ghrelin concentrations in O-NW were significantly lower than those present in Y-NW and superimposable on those of OB. The mean fasting plasma ghrelin concentrations in all groups of subjects were negatively correlated with body mass index and serum insulin levels, but not with TSH and IGF-I levels. This study provides evidence of an age-related decline of plasma ghrelin concentrations, which might explain, at least partially, the somatotroph dysregulation and the anorexia of the elderly subject.

Adolescent↗
PubMed2001

Production of IL-6 by human myoblasts stimulated with Abeta: relevance in the pathogenesis of IBM.

OBJECTIVE: To determine whether amyloid-beta protein (Abeta) can induce the production of proinflammatory cytokines by cultured normal muscle cells. BACKGROUND: Sporadic inclusion body myositis (IBM) is characterized by the presence of rimmed vacuoles and fibrillary inclusions of Abeta in muscle fibers, and often inflammatory cells. Endomysial expression of proinflammatory molecules has suggested an ongoing immune process, but the site of sensitization and the mechanisms that trigger an inflammatory reaction is unknown. METHOD: The authors used Northern blot analysis and specific immunoassays to study the expression and secretion in cell-free supernatants of tumor necrosis factor-alpha (TNFalpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) by purified human myoblasts and C2C12 mouse skeletal muscle cells incubated with Abeta[1-42] or Abeta[25-35] peptides. RESULTS: Nonstimulated muscle cells produced detectable IL-6, whereas secretion of IL-1beta and TNFalpha was absent. Incubation with Abeta peptides increased IL-6 production, whereas TNFalpha and IL-1beta levels remained undetectable. Northern blot analysis of Abeta-stimulated human myoblasts revealed an increase in IL-6 mRNA expression. CONCLUSIONS: Cultured muscle cells increase the constitutive production of IL-6 in response to local deposition of Abeta in sporadic IBM. IL-6 could be a CD8(+) proliferation and differentiation agent, an autocrine proteolysis-inducing factor of damaged myotubes, and a proliferation-stimulating agent for satellite cells to replace the destroyed myofibers in IBM.

Adult↗
PubMed2001

[Left atrial thrombosis in patients with antiphospholipid antibody syndrome and mesenchymal abnormal septum].

Antiphospholipid antibodies are a heterogeneous family of immunoglobulins that includes lupus anticoagulant and anticardiolipin antibodies. They are strongly associated with a clinical syndrome characterized by venous and arterial thrombosis and spontaneous fetal losses. This syndrome may be primary or else secondary to autoimmune or neoplastic diseases. The cardiovascular system is frequently involved with mitral or aortic insufficiency, juvenile myocardial infarction, and primitive pulmonary hypertension. However, the occurrence of intracardiac thrombi is rare. We describe a case of an intracardiac right atrial thrombus in a 19-year-old asymptomatic woman who was admitted in December 1998 to the Thrombosis Center owing to the finding, during routine work-up, of a prolonged activated partial thromboplastin time (71 s) and thrombocytopenia (71 x 1000/mm3), a positive antinuclear antibody test (1/320), positivity for lupus anticoagulant, and increased IgG (92 GPL-U/ml) and IgM (27 MPL-U/ml) anticardiolipin antibodies. Six months later, the patient presented with headache, edema and cyanosis of the face and jugular swelling. Transthoracic and transesophageal echocardiography revealed a right atrial mass which was clearly distinguishable from the tricuspid valve and extended to the superior vena cava. The patient was successfully submitted to surgical excision of the thrombus. Histology revealed that the mass was adherent to an abnormal septum consisting of mesenchymal tissue. Although the American Rheumatology Association criteria for the diagnosis of systemic lupus erythematosus were not fulfilled, the positivity of antinuclear antibody test is in favor of a lupus-like syndrome. The decision to opt for surgical excision of the thrombus was determined by the unclear nature of the atrial mass. It may be necessary that such patients be submitted to anticoagulant therapy for the rest of their lives or temporarily (6-12 months). This underscores the importance of the anatomical abnormality as a promoting factor. Transthoracic echocardiography (as well as transesophageal echocardiography in selected cases) must be considered as an essential component of the initial diagnostic work-up in patients presenting with antiphospholipid antibodies.

Adult↗
PubMed2000

The human astrocytoma cell line U373MG produces monocyte chemotactic protein (MCP)-1 upon stimulation with beta-amyloid protein.

Astrocytes associated with beta-amyloid (Abeta) accumulate in senile plaques of Alzheimer's disease (AD). To investigate the biological effects of Abeta/astrocyte interaction, we examined chemokine production by the human astrocytoma cell line U373MG stimulated with Abeta peptides. Northern blot analysis and specific immunoassays demonstrate that Abeta [1-42] and Abeta [25-35] induce mRNA expression and release of monocyte chemotactic protein (MCP)-1 but not of gamma-interferon inducible protein (IP)-10 by U373MG cells. The observation that Abeta induces astrocyte production of the potent microglia chemoattractant MCP-1 contributes to understanding mechanism of damage exerted by Abeta in AD senile plaques.

Amyloid beta-Peptides↗
PubMed2000

Synergistic effect of beta-amyloid protein and interferon gamma on nitric oxide production by C2C12 muscle cells.

Nitric oxide (NO) is an important mediator of diverse physiological and pathological responses. NO-induced oxidative stress has been proposed in the pathogenesis of muscle tissue damage in inclusion-body myositis (IBM), which is characterized by deposition of beta-amyloid protein (Abeta) in vacuolated muscle fibres. To determine whether Abeta can induce NO production in skeletal muscle, we stimulated C2C12 mouse skeletal muscle cells in vitro with Abeta[1-42] or Abeta[25-35] peptides in the presence or absence of interferon gamma (IFN-gamma). Neither Abeta peptides nor IFN-gamma were able to stimulate nitrite (NO(2)(-)) production by C2C12 cells when given alone. However, combination of IFN-gamma with either Abeta[1-42] or Abeta[25-35] resulted in significant NO(2)(-) release into cell-free supernatants. Northern blot analysis of RNA obtained from Abeta/IFN-gamma-stimulated C2C12 cells revealed increased mRNA accumulation of inducible nitric oxide synthase (iNOS). Moreover, approximately 4% of muscle cells incubated with Abeta peptides and IFN-gamma showed ultrastructural features of DNA fragmentation. These findings, taken together, indicate that the association of Abeta with IFN-gamma stimulates NO(2)(-) production via induction of iNOS gene expression in skeletal muscle cells, with occasional evidence for nuclear changes suggesting apoptotic morphology. These data further support a role for Abeta deposition in the pathogenesis of postulated oxidative damage in IBM.

Amyloid beta-Peptides↗
PubMed1999

Alpha-MSH peptides inhibit production of nitric oxide and tumor necrosis factor-alpha by microglial cells activated with beta-amyloid and interferon gamma.

Alpha-melanocyte stimulating hormone (alpha-MSH) is an ancient tridecapeptide with potent inhibitory activity in all major forms of inflammation. The anti-inflammatory message sequence of alpha-MSH resides in the COOH-terminal tripeptide alpha-MSH[11-13]. We tested the influence of alpha-MSH[1-13] and of alpha-MSH[11-13] in a cultured murine microglia cell line known to produce nitric oxide (NO(-)(2)) and tumor necrosis factor (TNFalpha) when stimulated with beta-amyloid protein (Abeta). Melanocortin peptides significantly inhibited release of both NO(-)(2) and TNFalpha into cell-free supernatants from microglia stimulated with Abeta[1-42] or Abeta[25-35] peptides and interferon gamma (IFNgamma). Northern blot analysis demonstrated that alpha-MSH[1-13] and alpha-MSH[11-13] inhibited accumulation of inducible nitric oxide synthase (iNOS) and TNFalpha mRNA was triggered by Abeta stimulation. Abeta/microglial interaction is believed to promote the progression of inflammatory and neurodegenerative changes in senile plaques in Alzheimer's disease. Our data indicate that alpha-MSH peptides might be used to modulate the local response of the brain to Abeta deposition in this neurodegenerative disease.

Amyloid beta-Peptides↗
PubMed1998

Melanocortin peptides inhibit production of proinflammatory cytokines and nitric oxide by activated microglia.

Inflammatory processes contribute to neurodegenerative disease, stroke, encephalitis, and other central nervous system (CNS) disorders. Activated microglia are a source of cytokines and other inflammatory agents within the CNS and it is therefore important to control glial function in order to preserve neural cells. Melanocortin peptides are pro-opiomelanocortin-derived amino acid sequences that include alpha-melanocyte-stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). These peptides have potent and broad anti-inflammatory effects. We tested effects of alpha-MSH (1-13), alpha-MSH (11-13), and ACTH (1-24) on production of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO) in a cultured murine microglial cell line (N9) stimulated with lipopolysaccharide (LPS) plus interferon gamma (IFN-gamma). Melanocortin peptides inhibited production of these cytokines and NO in a concentration-related fashion, probably by increasing intracellular cAMP. When stimulated with LPS + IFN-gamma, microglia increased release of alpha-MSH. Production of TNF-alpha, IL-6, and NO was greater in activated microglia after innmunoneutralization of endogenous alpha-MSH. The results suggest that alpha-MSH is an autocrine factor in microglia. Because melanocortin peptides inhibit production of pro-inflammatory mediators by activated microglia they might be useful in treatment of inflammatory/degenerative brain disorders.

Adrenocorticotropic Hormone↗
PubMed1994

[Effectiveness of nasal positive pressure ventilation in the management of acute refractory left ventricular insufficiency].

BACKGROUND: Ehen refractory to optimal medical treatment cardiogenic pulmonary edema requires mechanical ventilation as a last therapeutic resource. In recent years an increasing number of authors reported their experience in the management of acute or subacute respiratory failure with non-invasive mechanical ventilation by nasal mask. MATERIALS AND METHODS: Encouraged by the first promising results reported in literature we experimented this new therapeutic tool in a first group of seven elderly patients (mean age: 76.57--range: 65-89); they all had been admitted for severe cardiogenic pulmonary edema unresponsive to maximal doses of the conventional drugs available for treating acute decompensated heart failure. The enrolled patients were treated with intermittent ventilation administered by nasal mask at selected values of inspiratory positive airway pressure (IPAP) that were comprised between 10 and 20 cm H2O. At the same time an expiratory positive airway pressure (EPAP) at values comprised between 3 and 8 cm H2O was applied. Ventilation was continued for variable periods of 3-24 hours until acceptable values of PaO2 and PaCO2 were obtained. The ventilation modality was spontaneous, spontaneous-time or timed depending on the patients' level of consciousness at starting time. RESULTS: A good short-term outcome was achieved in all the patients regardless of the ventilation modality applied. The main blood gas alteration was severe hypercapnia with acidosis in three patients, while the other four presented critical hypoxemia unresponsive to simple oxygen supply even if delivered by high-flow Venturi mask. Four of our seven patients were discharged from hospital in satisfactory haemodynamic conditions; the remaining three died during hospitalization from refractory heart failure. CONCLUSIONS: In this our preliminary experience the therapeutic approach with nasal positive pressure ventilation (NPPV) and EPAP proved to be very effective to improve the signs and symptoms of acute refractory cardiogenic pulmonary edema as it avoided the need of invasive mechanical ventilation. It was well tolerated by all our patients; besides it was not difficult to use or time-consuming for physician and nurses. On the other hand it didn't modify our patients' medium or long-time prognosis which was strictly related to their preexisting left ventricular pump derangement.

Administration, Intranasal↗
PubMed1994

[Recovery of pump function in ischemic hypokinetic cardiopathy subjects treated with weekly intermittent infusion of dobutamine. A clinical case].

The case is reported of a 69-year-old man with refractory heart failure due to ischemic cardiomyopathy. All other available treatments having failed and 250 mg doses of furosemide having been administered without success, dobutamine infusion was tried, at first with 72 hours of continuous infusion of 5 mcg/kg/min, followed by intermittent infusion at the same dosage, first with 12-h intervals, subsequently at the rate of 2-3 infusions weekly, and finally, after about 50 days, with a single weekly infusion. Clinical and hemodynamic results were brilliant with the patient passing from grade IV NYHA to grade II and from ejection fraction 21% (Teichholz M-mode measurement) to 55%, 14 months after the start of dobutamine treatment. Discussing the possible mechanisms of this favourable result, the authors stress the possible improvement of the contractility of the "stunned" or "hibernating" myocardial segments. On the basis of their experience and of data in the literature the authors underline the validity of a therapeutic protocol of intermittent dobutamine infusion for severe heart failure.

Aged↗
PubMed1993

Intraocular and plasma kinetics of tenoxicam in rabbits.

Non-steroidal anti-inflammatory drugs (NSAID) represent potentially useful agents in the treatment of a number of ocular pathologies, but their intraocular penetration and distribution have not yet been reported. With the aim of clarifying this point, we evaluated the concentrations of the well known NSAID, tenoxicam, in the aqueous and vitreous humors of rabbits treated i.m. with the drug (7 mg/kg). The tenoxicam kinetics in these ocular fluids followed that in plasma with the time-to-peak shifted to higher values in the vitreous (1 h) as compared to that in the aqueous and plasma (40 min). AUC was also higher in the vitreous (10.4 micrograms.h/ml) than in the aqueous humor (2.8 micrograms.h/ml).

Animals↗