The PU.1 transcription factor induces cyclin D2 expression in U937 cells.
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Cyclin D2↗
Biomedical subjects
A Messina
Publications and source records attributed to A Messina.
New model of liver regeneration induced through use of vascular endothelial growth factor.
INTRODUCTION: Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen. The objective of this study was to verify the proregenerative effects of VEGF in an experimental model of acute liver failure. MATERIALS AND METHODS: Sixty four rats that underwent intraperitoneal injection of carbon tetrachloride (CCl(4)) were randomly divided into two groups: group B animals received intravenous injection of VEGF(164) 1 hour following CCl(4) poisoning. Group A hosts were untreated. To obtain daily liver function tests (LFTs) and histological samples, on each day up to 8 days we sacrificed four rats in each group. RESULTS: The laboratory examinations showed notable alteration of LFTs in group A, while group B revealed only slight changes. The histological examination showed greater liver damage in group A compared with group B. CONCLUSION: Our results suggest that administration of exogenous VEGF protects the liver from CCl(4)-induced acute hepatic failure. Further studies are underway to assess whether exogenous VEGF is effective in other liver injuries.
Alanine Transaminase↗
Coherent control of stimulated emission inside one-dimensional photonic crystals.
In this paper, the quasinormal mode (QNM) theory is applied to discuss the quantum problem of an atom embedded inside a one-dimensional (1D) photonic band gap (PBG) cavity pumped by two counterpropagating laser beams. The e.m. field is quantized in terms of the QNMs in the 1D PBG and the atom modeled as a two-level system is assumed to be weakly coupled to just one of the QNMs. The main result of the paper is that the decay time depends on the position of the dipole inside the cavity, and can be controlled by the phase difference of the two laser beams.
Journal Article↗
Scaling of non-Markovian Monte Carlo wave-function methods.
We demonstrate a scaling method for non-Markovian Monte Carlo wave-function simulations used to study open quantum systems weakly coupled to their environments. We derive a scaling equation, from which the result for the expectation values of arbitrary operators of interest can be calculated, all the quantities in the equation being easily obtainable from the scaled Monte Carlo wave-function simulations. In the optimal case, the scaling method can be used, within the weak coupling approximation, to reduce the size of the generated Monte Carlo ensemble by several orders of magnitude. Thus, the developed method allows faster simulations and makes it possible to solve the dynamics of the certain class of non-Markovian systems whose simulation would be otherwise too tedious because of the requirement for large computational resources.
Journal Article↗
Action of prolactin, IFN-gamma, TNF-alpha and LPS on heme oxygenase-1 expression and VEGF release in human monocytes/macrophages.
The pituitary hormone prolactin (PRL) has recently been regarded as a local regulator of macrophage responses. Our goal in this study was to investigate the regulatory interaction between PRL, interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS) in the heme oxygenase-1 (HO-1) expression and the vascular endothelial growth factor (VEGF) production in human monocytes/macrophages (HMMs). In vitro treatment of HMMs with PRL, IFN-gamma, TNF-alpha and LPS was found to increase both HO-1 expression and protein synthesis in a time-dependent manner. HMMs treated with PRL, IFN-gamma, TNF-alpha and LPS also showed an enhanced release of VEGF. Moreover, co-stimulation of PRL with LPS caused activation of HMMs functions, enhancement of HO-1 expression and induction of VEGF release, whereas addition of PRL inhibited up-regulation of HO-1 or VEGF induced by IFN-gamma or TNF-alpha. Our results demonstrate that PRL, IFN-gamma, TNF-alpha and LPS modulate the expression of angiogenic factors providing additional information about the regulatory mechanism, which controls the angiogenic function of macrophages.
Heme Oxygenase (Decyclizing)↗
Simultaneous presentation of meningiomas with other intracranial tumours.
Fifteen patients with simultaneous presentation of meningiomas with other intracranial tumours are reviewed. The associated tumours included a brain metastasis in six cases, glioma in three, pituitary adenoma in two, craniopharyngioma in one,acoustic schwannoma in two and brain lymphoma in one. A correct preoperative radiological diagnosis was made in 12 patients; in three others the associated tumour was discovered at operation and by histological studies. A one-stage removal of both tumours through the same approach was performed in nine patients, whereas six others underwent two-stage operations with an interval of 1 - 13 months. The literature relating to meningiomas associated with other intracranial tumours is reviewed and the possible pathogenetic correlations are discussed. A diagnostic pitfall may occur for metastasis into a meningioma, glioma surrounding a meningioma and different suprasellar lesions. The surgical indication and management of meningiomas may be significantly influenced by the presence of another different intracranial tumour.
Adult↗
Ribavirin up-regulates IL-12 p40 gene expression and restores IL-12 levels in Leishmania-treated PBMCs.
Ribavirin, a nucleoside analogue that interferes with viral mRNA synthesis and inhibits the replication of RNA and DNA viruses, has been recently proposed as an effective immune response modulator. In the present report, we studied the effect of ribavirin on IL-12 p40 gene expression in peripheral blood mononuclear cells (PBMCs) of healthy subjects. We also studied ribavirin effects on PBMCs activated with lipopolysaccharide (LPS) and phytohaemagglutinin (PHA) and treated with Leishmania donovani antigens. We provide evidence that ribavirin was able to up-regulate IL-12 p40 gene expression and to restore levels of IL-12 p40 gene expression and IL-12 secretion in fully activated PBMCs that were strongly inhibited by L. donovani antigens. Because effective management of leishmanial disease is usually associated with a prevalent T-helper 1 immune response with elevated production of IL-12,our preliminary results may be of particular interest, provided that they will be confirmed by further in vitro and in vivo studies, when considering a possible use of ribavirin as adjuvant in severe leishmanial disease.
Adolescent↗
Second quantization and atomic spontaneous emission inside one-dimensional photonic crystals via a quasinormal-modes approach.
An extension of the second quantization scheme based on the quasinormal-modes theory to one-dimensional photonic band gap (PBG) structures is discussed. Such structures, treated as double open optical cavities, are studied as part of a compound closed system including the electromagnetic radiative external bath. The electromagnetic field inside the photonic crystal is successfully represented by a new class of modes called quasinormal modes. Starting from this representation we introduce the Feynman's propagator to calculate the decay rate of a dipole inside a PBG structure, related to the density of modes, in the presence of the vacuum fluctuations outside the one-dimensional cavity.
Journal Article↗
Prolactin increases HO-1 expression and induces VEGF production in human macrophages.
The pituitary hormone prolactin (PRL) is a multifunctional polypeptide which exerts a role on cell proliferation and may also contribute to cell differentiation. PRL is also produced by immune cells and is regarded as a key component of the neuroendocrine-immune loop and as a local regulator of macrophage response. The involvement of PRL in regulating monocyte/macrophage functions is suggested by the presence of PRL receptors in these cells. It has been shown that PRL possess both angiogenic and antiangiogenic effects. Recently, we revealed that augmentation of HO-1 activity enhances PRL-mediated angiogenesis in human endothelial cells. Since macrophages are key participants in angiogenesis our objective was to investigate the effect of PRL also in human macrophages. In vitro treatment of macrophages with PRL was found to increase both heme oxygenase-1 (HO-1) expression and protein synthesis in a time and dose dependent manner as quantified respectively by reverse-transcriptase real-time polymerase chain reaction and Western blot analysis. PRL-treated macrophages also showed an enhanced release of vascular endothelial growth factor (VEGF) as demonstrated by ELISA assay. Furthermore, to determine whether PRL-induced HO-1 activity was required for VEGF production by macrophages, the effect of PRL on the induction of VEGF was studied in the presence of an inducer stannic chloride (SnCl(2)) and of an inhibitor stannic mesoporphyrin (SnMP) of HO activity. Our observations suggest that PRL may regulate monocyte activation and influences not only immune function but also angiogenesis.
Blotting, Western↗
Prolactin induces chitotriosidase gene expression in human monocyte-derived macrophages.
Human chitotriosidase (Chit), a chitinolytic enzyme, is a member of the chitinase family. In human's plasma Chit activity have been proposed as a biochemical marker of macrophage activation in several lysosomal diseases. Recently we found that Chit activity is higher in patients affected by Plasmodium falciparum malaria infection suggesting that chitotriosidase may induce an immunological response. The pituitary hormone prolactin (PRL) is a multifunctional polypeptide also produced by immune cells and represents a key component of the neuroendocrine-immune loop. The presence of PRL receptors in macrophage suggests that PRL is involved in regulating functions in these cells. Our objective in this study was to investigate the effect of PRL in human monocyte-derived macrophages (HMMs) on Chit production. Administration of PRL in HMMs was found to increase both expression and activity of Chit in a time and dose dependent manner as quantified, respectively, by real time PCR and Chit activity assay. PRL-treated monocyte-derived macrophages showed also an enhanced release of superoxide anion (O2-) release. Our observations confirm that PRL regulates HMMs activation and suggest, for the first time, that it influences immune function also through the induction of Chit activity.
Cells, Cultured↗
HPLC study of tyrosinase inhibition by thiopronine.
Thiopronine (N-2-mercaptopropionyl-glycine, NMPG) inhibits the o-dihydroxy-phenolase activities of mushroom tyrosinase. When d,l-3-4-dihydroxyphenylalanine (DOPA) is employed as substrate, the inhibition was found to be a competitive-type with K(i) of 0.95 micro m. We found in addition that thiopronine interacts with the enzymatic generated product (o-quinone) to form a colourless conjugate compound causing an apparent inhibition. These data suggest that thiopronine inhibits mushroom tyrosinase activity in two ways: (1) by forming an adduct with dopaquinone; and (2) by direct interaction with the enzyme probably towards the copper (II) present in the active site or cysteine-rich domains. This finding was indicated by the presence of a lag period prior to the attainment of an inhibited steady-state rate. Both lag period and steady-state rate were dependent on thiopronine and substrate concentrations. An increase of thiopronine concentration causes longer lag periods as well as a concomitant decrease in the tyrosinase activity. The presence of an excess of copper (II) reverses the inhibition exerted by thiopronine.
Agaricales↗
Hemorrhagic vascular complications of endoscopic transsphenoidal surgery.
Two hundred and fifty consecutive patients operated on by an endoscopic endonasal transsphenoidal approach were retrospectively analyzed in order to evaluate hemorrhagic vascular complications occurring during or after the surgical procedure and their appropriate management. Vascular complications of endoscopic transsphenoidal surgery are identical to those of a microsurgical transsphenoidal approach. Damage to the sphenopalatine artery and to the internal carotid artery (ICA), which are the most frequent vascular troubles, may require technical tricks because of some aspects connected to the approach itself and of the physical properties of the endoscope. Furthermore, the progress in interventional neuroradiology in the last decades offers new solutions in respect to the past, where the use of the surgical microscope was already a tremendous progress. The anatomic substrate of each complication is discussed, along with the peculiar surgical details related to it.
Carotid Artery, Internal↗
[Innovative use of the vascular endothelial growth factor in an experimental model of acute liver failure].
Vascular Endothelial Growth Factor (VEGF) is an endothelial cell mitogen and an important stimulator of sinusoidal endothelial cell proliferation. The aim of this research was to study the effects of exogenous VEGF in a rat model of acute liver failure. The study was conducted on 64 rats (240-300 g). All rats underwent intraperitoneal injection (5 ml/kg) of 25% carbon tetrachloride (CCl4) and 75% paraffin oil. This dosage of CCl4 was devised to induce nonfatal acute liver failure with spontaneous recovery in 7 days. The animals were randomly divided into 2 groups. Group B animals underwent i.v. injection of 200 ng of VEGF165 one hour following intra-peritoneal injection of CCl4. To obtain daily liver functional tests (LFTS) and histological liver samples, 4 rats in each group were sacrificed daily up to 8 days. In group A, the liver histology showed massive periportal hepatocyte necrosis associated with portal lymphocytic infiltrates. The peak of the damage was documented at 72 hours following CCl4. Group B showed minimal necrosis, moderate periportal edema and a minimum periportal steatosis. At 48 hours steatotic changes had disappeared and the periportal edema was resolving. LFTs demonstrated severe liver damage in rats in group A. In group A the peak AST (mean 322.5 IU/L) and ALT (mean 250.25 IU/L) were recorded at 72 hours. In group B, at 72 hours the mean AST was 137 IU/L (normal < 95 IU/L) and ALT 68 IU/L(normal < 45 IU/L). The maximum levels of AST and ALT, in group B, were 152.3 IU/L and 72.3 IU/L, at 24 hours. According to our results exogenous VEGF successfully protects the liver from CCl4 induced acute liver failure. Further studies will demonstrate if exogenous VEGF can be effective in other liver injuries.
Animals↗
Modulation of immune response in Plasmodium falciparum malaria: role of IL-12, IL-18 and TGF-beta.
The interaction between pro- and anti-inflammatory cytokines such as interleukin 12 (IL-12), interleukin 18 (IL-18) and transforming growth factor beta (TGF-beta) plays an important role in malaria pathogenesis and outcome, modulating the immunoresponse in Plasmodium falciparum malaria. In our previous studies, we analyzed the plasmatic levels of IL-12, IL-18 and TGF-beta in 105 African children with different degrees of malaria and we correlated the production of these cytokines with the severity of the disease. The aim of the present study was to analyze with a mathematical model, taking into account all the relationships between these cytokines and the parameter variations involved in malaria pathogenesis that influence the results of each type of treatment or therapeutic protocol on patients at different stages of the disease. A mathematical correlation was demonstrated between the levels of pro-inflammatory and anti-inflammatory cytokines, and from this it was possible to build curves of reference in which each patient was positioned based on IL-12 level. Our data, obtained in patients with mild and severe diseases, demonstrate that the levels of IL-12 represent a reliable parameter to predict the progression of the disease, which may be complemented or modulated by administration of IL-18 and TGF-beta. Our findings provide future implications for an immune therapy against the P. falciparum malaria infection, especially in the early phase of the disease showing that a more aggressive outcome may be due to the lack of a balanced immune response.
Animals↗
Persistent high plasma levels of interleukins 18 and 4 in children with recurrent infections of the upper respiratory tract.
The aim of this study was to examine whether children with recurrent infections of the upper respiratory tract might have alterations in the systemic immune response to viral infections as compared with healthy control children. We quantitated plasma levels of interferon-gamma, interleukin-12, interleukin-18, interleukin-4, lymphocyte subpopulations, serum immunoglobulins, and subclasses of immunoglobulin G in 30 children under the age of 6 years with recurrent infections of the upper respiratory tract, both during the acute phase of the infection and 4 weeks later, when clinical symptoms had resolved, as well as in 20 normal controls. We found elevated levels of immunoglobulin G primarily due to increased levels of immunoglobulin G(1). Moreover, significantly higher levels of interleukin-18 and interleukin-4 were noted during the acute phase of infection among children with an increased incidence of respiratory infections as compared with the controls (P =.022 and P =.0001, respectively), while plasma levels of interferon-gamma and interleukin-12 were significantly lower (P =.034 and P =.0001, respectively) than in controls. We suggest that an imbalance between T-cell helper type-1 and T-cell helper type-2 immune responses might be responsible for the perpetuation of recurrent infections of the upper respiratory tract.
Child, Preschool↗
Cell death in human acute myelogenous leukemic cells induced by pyrrolidinedithiocarbamate.
Pyrrolidinedithiocarbamate (PDTC) is a metal chelating compound, which exerts both pro-apoptotic effect and pro-oxidant activity on many cells. Our objective was to investigate whether PDTC was able to interfere with apoptotic process in leukemic and normal bone marrow CD34+ cells. Since hematopoietic growth factors stimulate growth and differentiation and prevent apoptosis, we therefore studied the effect of growth factors pretreatment, such as interleukin-3 and granulocyte-macrophage colony stimulating factor, in human myeloid CD34+ cells to evaluate whether they protect the cells from the apoptotic action of PDTC. We revealed that PDTC exerted an apoptotic effect in leukemic CD34+ cells. This effect was dependent on the ability of this compound to generate the oxidation of cellular glutathion to its disulphide and consequently to induce an intracellular oxidative stress. Hematopoietic growth factors did not protect cells from apoptosis induced by previous treatment with PDTC. The ability of PDTC to induce apoptosis was restricted to acute myelogenous leukaemia CD34+ cells, since normal CD34+cells were insensitive to the pro-oxidant effect of PDTC. These findings imply that normal cells are equipped with mechanisms by which they respond differently to PDTC effects with respect to leukemic cells.
Antigens, CD34↗
Involvement of interferon regulatory factor-1 in monocyte CD95 expression and CD95-mediated apoptosis.
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Apoptosis↗
Serum concentrations of the interferon-gamma-inducible chemokine IP-10/CXCL10 are augmented in both newly diagnosed Type I diabetes mellitus patients and subjects at risk of developing the disease.
AIMS/HYPOTHESIS: Chemokines are chemotactic cytokines controlling the recruitment of leukocytes from the blood by regulating integrin adhesiveness. It has been shown that the migration of CD4+Th1 and CD4+Th2 cells is governed by specific chemokines. Increasing evidence suggests that the CD4+Th1 cheomoattractant chemokine CXCL10, also termed Interferon (IFN)-gamma -inducible protein (IP)-10 is pathogenetically involved in several immunoinflammatory and autoimmune diseases. METHODS: IFN-gamma and IP-10 were quantified by solid-phase ELISA in sera of patients with either newly diagnosed or long-term Type I (insulin-dependent) diabetes mellitus, and in sera of their healthy first degree relatives. The latter were subdivided into "low" and "high" risk prediabetic subjects depending on whether they were negative or positive for the anti-beta-cell autoantibodies ICA and GAD. RESULTS: Compared with healthy control subjects (18%, 9/50), those with a low risk of disease (21%, 5/24) and the group of patients with long-term Type I diabetes (24%, 12/50), IP-10 was found more frequently and at increased concentrations in both newly diagnosed Type I diabetic patients (84%, 42/50) and in those with a high risk of disease (73%, 16/22); in the latter, the IP-10 concentrations correlated with those of IFN-gamma. CONCLUSION/INTERPRETATION: Circulating IP-10 concentrations is increased in patients with Type I diabetes, but only during the early and subclinical stage of the disease.
Adult↗