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A Bacci

Publications and source records attributed to A Bacci.

At least 37 records · Page 2Linked to original sources

Synaptic and intrinsic mechanisms shape synchronous oscillations in hippocampal neurons in culture.

We have detected spontaneous, synchronous calcium oscillations, associated with variations in membrane potential, in hippocampal neurons maintained in primary culture. The oscillatory activity is synaptically driven, as it is blocked by tetrodotoxin, by the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and by toxins inhibiting neurotransmitter release from presynaptic nerve endings. Neuronal oscillations do not require for their expression the presence of a polyneuronal network and are not primarily influenced by the gamma-aminobutyric acid (GABA(A)) receptor antagonist picrotoxin, suggesting that they entirely rely on glutamatergic neurotransmission. Synaptic and intrinsic conductances shape the synchronized oscillations in hippocampal neurons. The concomitant activation of N-methyl-D-aspartate (NMDA) receptors and voltage-activated L-type calcium channels allows calcium entering from the extracellular medium and sustaining the long depolarization, which shapes every single calcium wave.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Astrocytes are required for the oscillatory activity in cultured hippocampal neurons.

Synchronous oscillations of intracellular calcium concentration ([Ca2+]i) and of membrane potential occurred in a limited population of glutamatergic hippocampal neurons grown in primary cultures. The oscillatory activity occurred in synaptically connected cells only when they were in the presence of astrocytes. Microcultures containing only one or a few neurons also displayed oscillatory activity, provided that glial cells participated in the network. The glutamate-transporter inhibitors L-trans-pyrrolidine-2, 4-dicarboxylic acid (PDC) and dihydrokainate, which produce an accumulation of glutamate in the synaptic microenvironment, impaired the oscillatory activity. Moreover, in neurons not spontaneously oscillating, though in the presence of astrocytes, oscillations were induced by exogenous L-glutamate, but not by the stereoisomer D-glutamate, which is not taken up by glutamate transporters. These data demonstrate that astrocytes are essential for neuronal oscillatory activity and provide evidence that removal of glutamate from the synaptic environment is one of the major mechanisms by which glial cells allow the repetitive excitation of the postsynaptic cell.

ATP-Binding Cassette Transporters↗

Interleukin-4 causes susceptibility to invasive pulmonary aspergillosis through suppression of protective type I responses.

Aspergillus fumigatus, an opportunistic fungal pathogen, causes multiple allergic and nonallergic airway diseases. Invasive pulmonary aspergillosis (IPA) is a nonallergic, life-threatening disease of immunocompromised patients. In a murine model of IPA, interleukin (IL)-4-deficient (IL-4-/-) BALB/c mice were used to examine the role of IL-4 in lung pathology and immune responses. IL-4-/- mice were more resistant than wild-type mice to infection caused by multiple intranasal injections of viable A. fumigatus conidia. Resistance was associated with decreased lung inflammatory pathology, impaired T helper (Th)-2 responses (including lung eosinophilia), and an IL-12-dependent Th1 response. In contrast, development of host-detrimental antifungal Th2 cells occurred in IL-12-/- and interferon-gamma-/- mice and in IL-4-/- mice when subjected to IL-12 neutralization. These results demonstrate that IL-4 renders mice susceptible to infection with A. fumigatus by inhibition of protective Th1 responses. IL-4 appears to have a distinct role in the pathogenesis of allergic and nonallergic lung diseases caused by the fungus.

Animals↗

IFN-gamma is required for IL-12 responsiveness in mice with Candida albicans infection.

To elucidate the role of IFN-gamma in antifungal CD4+ Th-dependent immunity, 129/Sv/Ev mice deficient for IFN-gamma receptor (IFN-gammaR(-/-)) were assessed for susceptibility to gastrointestinal or systemic Candida albicans infection and for parameters of innate and adaptive T helper immunity. IFN-gammaR(-/-) mice failed to mount protective Th1-mediated acquired immunity upon mucosal immunization or in response to a live vaccine strain of the yeast. The impaired Th1-mediated resistance correlated with defective IL-12 responsiveness, but not IL-12 production, and occurred in the presence of an increased innate antifungal resistance. The development of nonprotective Th2 responses was observed in IFN-gammaR(-/-) mice upon mucosal infection and subsequent reinfection. However, under experimental conditions of Th2 cell activation, the occurrence of Th2 cell responses was similar in IFN-gammaR(-/-) and in IFN-gammaR(+/+) mice. These results indicate the complex immunoregulatory role of IFN-gamma in the induction of mucosal and nonmucosal anticandidal Th cell responses; IFN-gamma is not essential for the occurrence of Th2 responses but is required for development of IL-12-dependent protective Th1-dependent immunity.

Animals↗

Endogenous interleukin 4 is required for development of protective CD4+ T helper type 1 cell responses to Candida albicans.

Interleukin (IL)-4-deficient mice were used to assess susceptibility to systemic or gastrointestinal Candida albicans infections, as well as parameters of innate and elicited T helper immunity. In the early stage of systemic infection with virulent C. albicans, an unopposed interferon (IFN)-gamma response renders IL-4-deficient mice more resistant than wild-type mice to infection. Yet, IL-4-deficient mice failed to efficiently control infection in the late stage and succumbed to it. Defective IFN-gamma and IL-12 production, but not IL-12 responsiveness, was observed in IL-4-deficient mice that failed to mount protective T helper type 1 cell (Th1)-mediated acquired immunity in response to a live vaccine strain of the yeast or upon mucosal immunization in vivo. In vitro, IL-4 primed neutrophils for cytokine release, including IL-12. However, late treatment with exogenous IL-4, while improving the outcome of infection, potentiated CD4(+) Th1 responses even in the absence of neutrophils. These findings indicate that endogenous IL-4 is required for the induction of CD4(+) Th1 protective antifungal responses, possibly through the combined activity on cells of the innate and adaptive immune systems.

Animals↗

Cytokine- and T helper-dependent lung mucosal immunity in mice with invasive pulmonary aspergillosis.

The role of cytokine- and T helper (Th)-dependent lung mucosal antifungal immunity in murine invasive pulmonary aspergillosis (IPA) was investigated. Intact or leukopenic DBA/2 mice were resistant or highly susceptible, respectively, to infection caused by multiple intranasal injections of viable Aspergillus fumigatus conidia. Resistance was associated with unimpaired innate antifungal activity of pulmonary phagocytic cells, concomitant with high-level production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 and the presence of interstitial lymphocytes producing interferon-gamma and IL-2. Conversely, production of TNF-alpha and IL-12 was down-regulated in highly susceptible mice, which also had defective innate antifungal immunity and high-level production of IL-4 and IL-10 by lung lymphocytes. Resistance was increased in susceptible mice upon local IL-4 or IL-10 neutralization or IL-12 administration. These results indicate that, similar to observations in mice with disseminated aspergillosis, innate and Th1-dependent immunity play an essential role in host defense against IPA.

Animals↗

Defective co-stimulation and impaired Th1 development in tumor necrosis factor/lymphotoxin-alpha double-deficient mice infected with Candida albicans.

To define the immunological functions of tumor necrosis factor (TNF) in Candida albicans infection, TNF/lymphotoxin (LT)-alpha double-deficient mice were assessed for susceptibility to systemic or gastrointestinal infection and parameters of innate and adaptive Th immunity. When compared to wild-type mice, TNF/LT-alpha-deficient mice were more susceptible to either type of infection caused by virulent or low-virulence C. albicans cells. Susceptibility to infection correlated with impaired development of protective Th1 responses, in spite of the production of bioactive IL-12. The occurrence of predominant Th2 responses was associated with both impaired antifungal effector functions of neutrophils and a defective expression of co-stimulatory molecules on macrophages. All functions were improved upon administration of recombinant TNF-alpha, also resulting in increased resistance to infection. These findings indicate that the protective effect of TNF-alpha in candidiasis relies on the induction of antifungal Th1 responses, possibly occurring through stimulation of antifungal effector functions and co-stimulatory activities of phagocytic cells.

Animals↗

Granulomatous hypophysitis caused by a ruptured intrasellar Rathke's cleft cyst: report of a case and review of the literature.

OBJECTIVE AND IMPORTANCE: Ruptured Rathke's cleft cyst is a rare cause of giant cell granulomatous hypophysitis. Chronic inflammatory reaction is caused by extravased cyst content into the adjacent gland. We provide a demonstration that mucins produced by cells lining the cyst wall caused the granulomatous giant cell reaction. CLINICAL PRESENTATION: A 37-year-old nonpregnant woman presented with a 3-year-history of headache and amenorrhea. She had experienced normal sexual maturation, and her medical history was unremarkable. Radiologically, the lesion appeared as an intrasellar mass with a cystic component indistinguishable from a pituitary adenoma with cystic degeneration. TECHNIQUE: The patient underwent a transsphenoidal approach. Because no demarcation between normal and affected tissue was evident at surgery, the lesion and residual pituitary were radically removed. Tissue was studied using routine hematoxylin and eosin and histochemical stainings for mucins and immunocytochemical techniques. CONCLUSION: This study demonstrates that mucins that had spilled out from the cyst caused the granulomatous reaction. Using computed tomography, magnetic resonance imaging, and gross inspection, distinction between granulomatous hypophysitis and pituitary adenoma was virtually impossible. Nevertheless, a granulomatous reaction of the pituitary gland should be suspected in a case of a sellar mass having a cystic area. In such cases, intraoperatory diagnosis on frozen sections is mandatory because adoption of a conservative treatment allows preservation of the gland.

Adult↗

A TTX-sensitive conductance underlying burst firing in isolated pyramidal neurons from rat neocortex.

Pyramidal neurons were acutely isolated from neocortex slices of 14- to 20-day-old rats and patch-clamped under physiological conditions. Current-clamp recordings revealed firing patterns corresponding to those previously reported in slices as regular spiking (RS) and intrinsically bursting (IB), i.e., single action potentials (AP), trains of regular spikes and bursts with depolarizing after-potentials (DAP). In IB neurons, intracellular perfusion with KF blocked the high-voltage-activated Ca2+ and the Ca(2+)-dependent K+ currents, revealing APs with a 10-30 ms shoulder at -35 mV (shoulder AP), which was the supporting plateau of the intraburst spikes. The use of the A channel blocker, 4-aminopyridine, caused a three-fold reduction in the AP repolarizing rate. A study of the de- and repolarizing rates modulating the spike shape (shoulder AP, burst or single APs) suggested that the percentage of available A channels could play a crucial role in burst formation. Blockade of the residual T-type Ca2+ current by Ni2+ did not inhibit the AP shoulder, whereas it was completely and reversibly inhibited by 30 nM TTX, which did not affect AP amplitude. The AP rising rate was only halved by 100 nM TTX. The data concerning the A channel-mediated burst formation and the role of the TTX-sensitive conductance have been successfully simulated in a model cell. We suggest that bursting is an intrinsic property of the membrane of neocortex neurons, and is sustained by TTX-sensitive slowly inactivating and/or persistent Na+ conductances.

Animals↗

[Breast carcinoma metastatic to meningioma: review of the literature and description of 2 new cases].

UNLABELLED: Two cases of breast carcinoma metastatic to meningioma are described in patients 69 and 62 years old respectively. MATERIAL AND METHODS: Cases were documented by radiological, histological and immunohistochemical techniques. RESULTS: Both meningiomas contained an invasive duct carcinoma of the breast, one of which was apocrine in nature. CONCLUSION: It is suggested that metastasis to meningioma is not so rare as it appears from the literature.

Aged↗

Neurons dissociated from neocortex fire with 'burst' and 'regular' trains of spikes.

Neurons acutely dissociated from neocortex slices of 14-16-day-old rats were patch-clamped in physiological conditions. Different pyramidal cells, spontaneously or in response to current steps, generate regular spiking and intrinsically bursting behaviour during long periods of time. We show that typical firing properties recorded in somatosensory neocortex slices are preserved in dissociated pyramidal neurons originating from the slices themselves, thus, providing a way for the related characterization of biophysical properties of currents in identified subtypes of pyramidal neurons.

Action Potentials↗

Outcome of teenage pregnancy in Maputo, Mozambique.

OBJECTIVE: To evaluate the perinatal outcome of teenage pregnancies in comparison with a population of older, high-risk women. METHOD: Data about 15,207 high-risk women delivered during 1989 at the Central Hospital of Maputo, Mozambique, were collected retrospectively from the clinical records. Of these women 2185 were less than 19 years old. Frequencies were compared through the chi 2-test or, when required, Fisher's exact test. Odds ratios and 95% confidence intervals were computed. RESULT: Frequency of operative vaginal deliveries (forceps and/or vacuum extraction), cesarean section rate and low birth rate were significantly higher among women under 19 than in the older ones. Also, maternal mortality and stillbirth rates were greater among teenagers, although the differences were not statistically significant. CONCLUSION: Among the selected, high-risk hospital population of a developing country young maternal age, both by itself and in association with other risk factors, represents an important predictor of adverse perinatal outcome for mothers and babies. Implications for family planning and reproductive education programs are discussed.

Adolescent↗