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Biomedical subjects

G Bernardi

Publications and source records attributed to G Bernardi.

At least 73 records · Page 4Linked to original sources
PubMed2005

Acanthocytosis as a predisposing factor for non-ketotic hyperglycaemia induced chorea-ballism.

BACKGROUND: Episodic non-ketotic hyperglycaemia in patients with diabetes may be responsible for a syndrome characterised by hemichorea-hemiballism associated with unique radiological features. OBJECTIVE: To investigate whether factors other than hyperglycaemia may be responsible for the neurological involvement. METHODS: Three patients who developed a persistent chorea-ballism syndrome triggered by a hyperglycaemic crisis were investigated. In these patients, the persistence of the involuntary movements required neuroleptic medication. RESULTS: T1 weighted magnetic resonance imaging revealed bilateral hyperintense lesions involving the striatum. Surprisingly, in these patients, the laboratory investigations revealed peripheral red blood cell acanthocytosis in a significant proportion of cells. CONCLUSION: Compared with the large population of patients with diabetes who do not show abnormal involuntary movements, unrecognised acanthocytosis in diabetes might render patients prone to develop hemichorea-hemiballism.

Aged↗
PubMed2004

Observation and properties of the X(3872) decaying to J/psipi(+)pi(-) in pp collisions at sqrt[s]=1.96 TeV.

We report the observation of the X(3872) in the J/psipi(+)pi(-) channel, with J/psi decaying to mu(+)mu(-), in pp collisions at sqrt[s]=1.96 TeV. Using approximately 230 pb(-1) of data collected with the Run II D0 detector, we observe 522+/-100 X(3872) candidates. The mass difference between the X(3872) state and the J/psi is measured to be 774.9+/-3.1(stat)+/-3.0(syst) MeV/c(2). We have investigated the production and decay characteristics of the X(3872) and find them to be similar to those of the psi(2S) state.

Journal Article↗
PubMed2004

Search for doubly charged higgs boson pair production in the decay to mu(+)mu(+)mu(-)mu(-) in pp collisions at sqrt[s]=1.96 TeV.

A search for pair production of doubly charged Higgs bosons in the process pp -->H(++)H(--) -->mu(+)mu(+)mu(-)mu(-) is performed with the D0 run II detector at the Fermilab Tevatron. The analysis is based on a sample of inclusive dimuon data collected at an energy of sqrt[s]=1.96 TeV, corresponding to an integrated luminosity of 113 pb(-1). In the absence of a signal, 95% confidence level mass limits of M(H(+/-+/-)(L))>118.4 GeV/c(2) and M(H(+/-+/-)(R))>98.2 GeV/c(2) are set for left-handed and right-handed doubly charged Higgs bosons, respectively, assuming 100% branching into muon pairs.

Journal Article↗
PubMed2004

CagA-positive Helicobacter pylori strains may influence the natural history of atherosclerotic stroke.

OBJECTIVE: To test the hypothesis that infection with virulent cytotoxin-associated gene-A (CagA)-bearing Helicobacter pylori strains influences the atherosclerotic process and the clinical course in atherosclerotic stroke patients. METHODS: ELISA was used to assess the seroprevalence of infection by H. pylori and CagA-positive strains in 185 patients. Intima-media thickness (IMT) was determined by Doppler ultrasound. Baseline, 1-week, and 1-month NIH Stroke Scale (NIHSS) scores were used to evaluate the short-term clinical course. RESULTS: H. pylori infection was found in 79% of patients; 58% of these tested positive for CagA. IMT was higher among CagA-positive patients than among CagA-negative ones (1.13 +/- 0.26 mm vs 0.97 +/- 0.15 mm; univariate analysis, p = 0.0001; multivariate analysis, odds ratio [OR], 2.36; 95% CI, 1.57 to 3.54; p = 0.0001) or H. pylori-negative ones (1.01 +/- 0.17 mm; univariate analysis, p = 0.007; multivariate analysis, OR, 1.90; 95% CI, 1.22 to 2.97; p = 0.005). CagA-positive patients had poorer initial outcomes based on serial measurements of the NIHSS score (repeated measures analysis of variance, p < 0.0001). No significant difference in IMT and NIHSS score was found between H. pylori-positive and H. pylori-negative patients. CONCLUSIONS: Infection with cytotoxin-associated gene-A-positive Helicobacter pylori strains in atherosclerotic stroke patients is associated with greater intima-media thickness and poorer short-term outcome compared with cytotoxin-associated gene-A-negative patients.

Aged↗
PubMed2004

Immunolocalization of CB1 receptor in rat striatal neurons: a confocal microscopy study.

Several lines of evidence indicate that cannabinoids, among other functions, are involved in motor control. Although cannabinoid receptors (CB(1)) mRNA has been observed in medium-sized spiny neurons of the striatum, a description of the precise localization of CB(1) at a protein level among striatal cells is still lacking. Therefore, we performed immunohistochemical studies with light and confocal microscopy to identify neuronal subpopulations that express CB(1) and to assess the distribution of the receptor within these neurons. In our single label light microscopy study, CB(1) was observed in most medium-sized neurons of the caudate-putamen. However, CB(1) was also present in large-sized neurons scattered throughout the striatum. Our dual-label study showed that 89.3% of projection neurons in matrix contain CB(1), and that 56.4% of projection neurons in patch are labeled for CB(1). To investigate the presence of CB(1) among the different subclasses of striatal interneurons we performed a double-labeling study matching CB(1) and each of the striatal interneuron markers, namely, choline acetyl-transferase, parvalbumin, calretinin, and nitric oxide synthase. Our double-label study showed that most parvalbumin immunoreactive interneurons (86.5%), more than one-third (39.2%) of cholinergic interneurons, and about one-third (30.4%) of the NOS-positive neurons are labeled for CB(1). Calretinin-immunolabeled neurons were devoid of CB(1).

Animals↗
PubMed2004

A precision measurement of the mass of the top quark.

The standard model of particle physics contains parameters--such as particle masses--whose origins are still unknown and which cannot be predicted, but whose values are constrained through their interactions. In particular, the masses of the top quark (M(t)) and W boson (M(W)) constrain the mass of the long-hypothesized, but thus far not observed, Higgs boson. A precise measurement of M(t) can therefore indicate where to look for the Higgs, and indeed whether the hypothesis of a standard model Higgs is consistent with experimental data. As top quarks are produced in pairs and decay in only about 10(-24) s into various final states, reconstructing their masses from their decay products is very challenging. Here we report a technique that extracts more information from each top-quark event and yields a greatly improved precision (of +/- 5.3 GeV/c2) when compared to previous measurements. When our new result is combined with our published measurement in a complementary decay mode and with the only other measurements available, the new world average for M(t) becomes 178.0 +/- 4.3 GeV/c2. As a result, the most likely Higgs mass increases from the experimentally excluded value of 96 to 117 GeV/c2, which is beyond current experimental sensitivity. The upper limit on the Higgs mass at the 95% confidence level is raised from 219 to 251 GeV/c2.

Journal Article↗
PubMed2004

Search for narrow tt resonances in pp collisions at square root of (s)=1.8 TeV.

A search for narrow resonances that decay into tt pairs has been performed using 130 pb(-1) of data in the lepton + jets channel collected by the Dphi detector in pp collisions at square root of (s)=1.8 TeV. There is no significant deviation observed from the standard-model predictions at a top-quark mass of 175 GeV/c2. We therefore present upper limits at the 95% confidence level on the product of the production cross section and branching fraction to tt for narrow resonances as a function of the resonance mass MX. These limits are used to exclude the existence of a leptophobic top-color particle with mass MX<560 GeV/c2, using a theoretical cross section for a width GammaX=0.012MX.

Journal Article↗
PubMed2004

A new SPG4 mutation in a variant form of spastic paraplegia with congenital arachnoid cysts.

The clinical and genetic findings are described for 16 patients from a large Italian family with a variant form of hereditary spastic paraplegia and congenital arachnoid cysts inherited as an autosomal dominant trait. A molecular study has revealed a novel missense mutation, T614I, in exon 17 of SPG4, which may play a role in both focal cortical dysgenesis and neurodegeneration of the motor neurons in the corticospinal tract.

Adenosine Triphosphatases↗
PubMed2004

Distribution of HIV-1 in the genomes of AIDS patients.

The localization of HIV-1 proviruses in compositional DNA fractions from 27 AIDS patients during the chronic phase of the disease with depletion of CD4+ and different levels of viremia showed the following. (1) At low viremia, proviruses are predominantly localized in the GC-richest isochores, which are characterized by an open chromatin structure; this result mimics findings on HIV-1 integration in early infected cells in culture. (2) At higher viremia, an increased distribution of proviruses in GC-poor isochores (which match the GC poorness of HIV-1) was found; this suggests a selection of cells in which the 'isopycnic' localization leads to a higher expression of proviruses and, in turn, to higher viremia. (3) At the highest viremia, integrations in GC-rich isochores are often predominant again, but generally not at the same level as in (1); this may be the consequence of new integrations from the extremely abundant RNA copies.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Localization of integrated adenovirus DNA in the hamster genome.

Adenovirus DNA integrated into the genomes of adenovirus-transformed hamster cells or of adenovirus type 12 (Ad12)-induced hamster tumor cells can be located at many different chromosomal sites. This raises the question as to whether distinct isochores of the hamster cell genome might be more accessible to recombination with adenovirus DNA. In Ad12- or Ad2-transformed hamster cell lines, and in Ad12 revertants, the investigated integrated viral DNA sequences were assigned to isochore families by analyzing DNA fractions from preparative CsCl density gradients for their buoyant densities (and, therefore, GC levels) and for the presence of viral DNA. Adenovirus DNA sequences were found in different isochores, which did not generally match the base composition of viral sequences. This is in apparent contrast to what was previously observed with retroviral integration. However, in cell lines carried in culture for many years, the viral DNA sequences might have been transposed to different isochore positions, since the host sequences flanking the viral DNA appear to have been conserved.

Adenoviridae↗
PubMed2004

Different TMS patterns of intracortical inhibition in early onset Alzheimer dementia and frontotemporal dementia.

OBJECTIVE: To investigate putative changes in cortical excitability of patients affected by early-onset mild dementia by means of transcranial magnetic stimulation (TMS) and to verify whether a peculiar neurophysiological profile may contribute to characterise Alzheimer's disease (AD) vs frontotemporal dementia (FTD). METHODS: Motor threshold and intracortical inhibition (ICI) and facilitation (ICF) after paired-pulse TMS (inter-stimulus intervals from 1 to 20 ms) were studied in two groups of early-onset demented patients with a neuropsychological profile suggestive of AD (n = 12) and FTD (n = 8). Twelve age-matched healthy subjects were considered as control group. In both patient groups, recordings were performed before and after a single oral dose of 4 mg galantamine. RESULTS: No significant difference in motor threshold was observed among the three studied groups. On the contrary, early-onset AD showed a significant reduction of ICI compared to control group, no changes were detected in FTD patients. No significant changes in ICF were found between both patient groups and healthy subjects. The acute administration of galantamine reversed the modified ICI in AD group. CONCLUSIONS: The differential pattern of ICI exhibited by early-onset AD vs FTD in the early stage of disease may represent a non-invasive, reproducible electrophysiological tool, which may contribute to early differential diagnosis and, possibly, to monitor therapeutic effectiveness. SIGNIFICANCE: The present results support the possibility that subtle, early modifications in intracortical circuitry features AD, but not FTD patients.

Aged↗
PubMed2004

Early ionic and membrane potential changes caused by the pesticide rotenone in striatal cholinergic interneurons.

Mitochondrial metabolism impairment has been implicated in the pathogenesis of several neurodegenerative disorders. In the present work, we combined electrophysiological recordings and microfluorometric measurements from cholinergic interneurons obtained from a rat neostriatal slice preparation. Acute application of the mitochondrial complex I inhibitor rotenone produced an early membrane hyperpolarization coupled to a fall in input resistance, followed by a late depolarizing response. Current-voltage relationship showed a reversal potential of -80 +/- 3 mV, suggesting the involvement of a potassium (K+) current. Simultaneous measurement of intracellular sodium [Na+]i or calcium [Ca2+]i concentrations revealed a striking correlation between [Na+]i elevation and the early membrane hyperpolarization, whereas a significant [Ca2+]i rise matched the depolarizing phase. Interestingly, ion and membrane potential changes were mimicked by ouabain, inhibitor of the Na+-K+ATPase, and were insensitive to tetrodotoxin (TTX) or to a combination of glutamate receptor antagonists. The rotenone effects were partially reduced by blockers of ATP-sensitive K+ channels, glibenclamide and tolbutamide, and largely attenuated by a low Na+-containing solution. Morphological analysis of the rotenone effects on striatal slices showed a significant decrease in the number of choline acetyltransferase (ChAT) immunoreactive cells. These results suggest that rotenone rapidly disrupts the ATP content, leading to a decreased Na+-K+ATPase function and, therefore, to [Na+]i overload. In turn, the hyperpolarizing response might be generated both by the opening of ATP-sensitive K+ channels and by Na+-activated K+ conductances. The increase in [Ca2+]i occurs lately and does not seem to influence the early events.

Animals↗
PubMed2004

Axotomy dependent purinergic and nitrergic co-expression.

Different lines of evidence indicate that ATP and nitric oxide (NO) play key roles in mediating neuronal responses after cell damage. Purinergic and nitrergic interactions have been proposed in non neural tissues physiological functions and, in different experimental models of brain injury, both purinergic and nitrergic activations have been reported. The present study was planned to ascertain possible relations of these two systems after brain damage. Variations in the expression of the nitric oxide synthase neuronal isoform (nNOS) enzyme, and of two subunits of purinergic ionotrophic receptors (P2X) namely P2X(1) and P2X(2) in precerebellar stations after cerebellar lesion in rats were analyzed and compared. After the lesion nNOS positive cells presented a clear increment followed by a decrement. Conversely, nNOS negative cells presented a rapid decrement in the first postlesional weeks that continued less pronounced afterward. Postlesional nNOS activation was related with time course of P2X(1) and P2X(2) activations. The capacity of the same cells to express both nNOS and P2X markers was investigated immunocytochemically. Confocal microscopy of double immunofluorescence showed a high percentage of co-localization among P2X(1)/nNOS, P2X(2)/nNOS and P2X(1)/P2X(2) in olivary and pontine neurons. In addition, NeuN/P2X(1) and NeuN/P2X(2) double immunofluorescence showed P2X(1) expressed only in neurons while P2X(2) expressed by both neurons and glia. Present data demonstrate that after cerebellar lesion nitrergic and purinergic systems are activated with similar time courses in precerebellar stations. Further, time differences in the relation between nNOS expression and cell survival suggest a multifarious role of NO in mediating cell reaction to axotomy. The tight cellular co-localization and temporal co-activation of purinergic and nitrergic markers indicate possible interactions between these two systems also in the CNS.

Animals↗
PubMed2004

Differential contribution of dopamine D2S and D2L receptors in the modulation of glutamate and GABA transmission in the striatum.

Compelling evidence indicates that the long (D2L) and the short (D2S) isoform of dopamine (DA) D2 receptors serve distinct physiological functions in vivo. To address the involvement of these isoforms in the control of synaptic transmission in the striatum, we measured the sensitivity to D2 receptor stimulation of glutamate- and GABA-mediated currents recorded from striatal neurons of three mutant mice, in which the expression of D2L and D2S receptors was either ablated or variably altered. Our data indicate that both isoforms participate in the presynaptic inhibition of GABA transmission in the striatum, while the D2-receptor-dependent modulation of glutamate release preferentially involves the D2S receptor. Accordingly, the inhibitory effects of the DA D2 receptor agonist quinpirole (10 microM) on GABA(A)-mediated spontaneous inhibitory postsynaptic currents (IPSCs)correlate with the total number of D2 receptor sites in the striatum, irrespective of the specific receptor isoform expressed. In contrast, glutamate-mediated spontaneous excitatory postsynaptic currents (EPSCs) were significantly inhibited by quinpirole only when the total number of D2 receptor sites, normally composed by both D2L and D2S receptors in a ratio favoring the D2L isoform, was modified to express only the D2S isoform at higher than normal levels. Understanding the physiological roles of DA D2 receptors in the striatum is essential for the treatment of several neuropsychiatric conditions, such as Parkinson's disease, Tourette's syndrome, schizophrenia, and drug addiction.

Animals↗
PubMed2003

PS1 Alzheimer's disease family with spastic paraplegia: the search for a gene modifier.

PS1 mutations are associated with classic Alzheimer's disease (AD); however, some families develop AD and spastic paraplegia (SP) with brain pathology characterized by Abeta cotton wool plaques. The authors report a variant AD family with the E280Q PS1 mutation. The fact that the same PS1 mutation can be found in patients with either variant or classic AD argues in favor of the presence of a genetic modifier. The authors have excluded that this modifier effect originates from coding sequence variations in three SP genes or from a second mutation in the other AD genes.

Alternative Splicing↗
PubMed2003

Search for large extra dimensions in the monojet+E(T) channel with the DØ detector.

We present a search for large extra dimensions (ED) in pp collisions at a center-of-mass energy of 1.8 TeV using data collected by the DØ detector at the Fermilab Tevatron in 1994-1996. Data corresponding to 78.8+/-3.9 pb(-1) are examined for events with large missing transverse energy, one high-p(T) jet, and no isolated muons. There is no excess observed beyond expectation from the standard model, and we place lower limits on the fundamental Planck scale of 1.0 and 0.6 TeV for 2 and 7 ED, respectively.

Journal Article↗
PubMed2003

Activation of beta1-adrenoceptors excites striatal cholinergic interneurons through a cAMP-dependent, protein kinase-independent pathway.

The role of noradrenergic neurotransmission was analyzed in striatal cholinergic interneurons. Conventional intracellular and whole-cell patch-clamp recordings were made of cholinergic interneurons in rat brain slice preparations. Bath-applied noradrenaline (NA) (1-300 microm) dose-dependently induced both an increase in the spontaneous firing activity and a membrane depolarization of the recorded cells. In voltage-clamped neurons, an inward current was induced by NA. This effect was not prevented by alpha-adrenoceptor antagonists, whereas it was mimicked by the beta-adrenoceptor agonist isoproterenol and blocked by the beta1 antagonists propranolol and betaxolol. Interestingly, forskolin, activator of adenylate cyclase, mimicked and occluded the membrane depolarization obtained at saturating doses of both dopamine and NA. Accordingly, SQ22,536, a selective adenylate cyclase inhibitor, reduced the response to NA. Analysis of the reversal potential of the NA-induced current did not provide homogeneous results, indicating the involvement of multiple membrane conductances. Because cAMP is known to modulate Ih, the effects of ZD7288, a selective inhibitor of Ih current, were examined on the NA-induced membrane depolarization/inward current. ZD7288 mostly reduced the response to NA. However, both KT-5720 and H-89, selective protein kinase A (PKA) blockers, failed to prevent the excitatory action of NA. Likewise, calphostin C, antagonist of PKC, genistein, inhibitor of tyrosine kinase, and 8-Bromo-cGMP, blocker of PKG, did not affect the response to NA. Finally, double-labeling experiments combining beta1-adrenoceptor and choline acetyltransferase immunocytochemistry by means of confocal microscopy revealed a strong beta1-adrenoceptor labeling on cholinergic interneurons. We conclude that NA depolarizes striatal cholinergic interneurons via beta1-adrenoceptor activation, through a cAMP-dependent but PKA-independent mechanism.

Adenylyl Cyclases↗